Beruflich Dokumente
Kultur Dokumente
School of Pharmacy
Georgina Heal, MD
Ryan M. Klein, MD
Scott T. Gallacher, MD
Guy Foster, MD
Michael Krutzik, MD
Farhad Mazdisnian, MD
Roham T. Zamanian, MD
Hans Poggemeyer, MD
H. L. Daneschvar, MD
S. E. Wilson, MD
College of Medicine
Phone: 800-331-8227
E-Mail: info@ccspublishing.com
Copyright 2003 Current Clinical Strategies Publishing. All rights reserved. This book, or
any parts thereof, may not be reproduced or stored in an information retrieval network
without the written permission of the publisher. The reader is advised to consult the drug
package insert and other references before using any therapeutic agent. No liability exists,
expressed or implied, for errors or omissions in this text. Current Clinical Strategies is a
registered trademark of Current Clinical Strategies Publishing Inc.
Printed in USA
ISBN 1-929622-16-3
Contents
Advanced Cardiac Life Support . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5
15
15
15
16
17
17
18
18
18
19
20
20
21
21
24
Cardiovascular Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Acute Coronary Syndromes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Myocardial Infarction and Unstable Angina . . . . . . . . . . . . . . . . . . . . . . .
Heart Failure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Atrial Fibrillation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Hypertensive Emergency . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Ventricular Arrhythmias . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Torsades de Pointes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Acute Pericarditis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Pacemakers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
25
25
25
32
36
41
44
44
45
46
Pulmonary Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Orotracheal Intubation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Nasotracheal Intubation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Ventilator Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Inverse Ratio Ventilation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Ventilator Weaning . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Pulmonary Embolism . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Asthma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Chronic Obstructive Pulmonary Disease . . . . . . . . . . . . . . . . . . . . . . . .
Pleural Effusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
49
49
50
51
52
52
54
58
62
65
Trauma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Pneumothorax . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Tension Pneumothorax . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Cardiac Tamponade . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Pericardiocentesis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
67
67
68
69
69
Hematologic Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Transfusion Reactions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Disseminated Intravascular Coagulation . . . . . . . . . . . . . . . . . . . . . . . . .
Thrombolytic-associated Bleeding . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
71
71
72
73
Infectious Diseases . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Bacterial Meningitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Pneumonia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Pneumocystis Carinii Pneumonia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Antiretroviral Therapy and Opportunistic Infections in AIDS . . . . . . . . . .
Sepsis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Peritonitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
75
75
79
83
85
87
91
Gastroenterology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 93
Variceal Bleeding . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 94
Acute Pancreatitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 99
Toxicology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Poisoning and Drug Overdose . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Toxicologic Syndromes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Acetaminophen Overdose . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Cocaine Overdose . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Cyclic Antidepressant Overdose . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Digoxin Overdose . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Ethylene Glycol Ingestion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Gamma-hydroxybutyrate Ingestion . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Iron Overdose . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Isopropyl Alcohol Ingestion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Lithium Overdose . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Methanol Ingestion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Salicylate Overdose . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Theophylline Toxicity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Warfarin (Coumadin) Overdose . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
105
105
106
106
108
109
109
110
111
111
112
112
113
113
114
115
Neurologic Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Ischemic Stroke . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Elevated Intracranial Pressure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Status Epilepticus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
117
117
120
122
125
125
127
130
133
134
135
136
140
141
Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 144
NO PULSE
Initia te CPR
If wi tnessed arrest, give
precord ial thump and
check pulse. If absent,
continue CP R
Ven tricular
fibrillation/tach ycardia
(VT/VF) p rese nt on
monitor?
NO
YES
Intu bate
Confirm tube pla ceme nt
Dete rmine rhythm and
cause.
VT/VF
Go to Fig 2
Arrh ythmia
Brad ycardia
Go to Fig 5
Tachycardia
Go to Fig 6
Electrical A ctivity?
YES
Pulseless e lectrical activity
Go to Fig 3
NO
Asystole
Go to Fig 4
Continue CPR
Secure IV access
In tubat e if no respo nse
Return of
spo nt ane ou s
circulation
Pu lseless E lectrical
Act ivity
Go to Fig 3
Asyst ole
Go to Fig 4
Co nt inue CP R
De fibrilla te 36 0 J, 30-60 seconds af te r ea ch dose of me dication
Repe at amio daro ne (Cord arone ) 15 0 mg IV P prn (if re urrent VF/ VT) , up to ma x
cu mulative do se of 22 00 mg in 24 ho urs
PULSELESSELECTRICALACTIVITY
ASYSTOLE
Consider bicarbonate1mEq/kg(1-2amp)if
hyperkalemia, acidosis, tricyclicoverdose.
Consider terminationof efforts.
Fig4- Asystole
BRADYCARDIA
Yes
No
Type II second degree AV heart
blockor third degree AV heart
block?
No
Observe
Yes
TACHYCARDIA
IMMEDIATE CARDIOVERSION
Atrial flutter 50 J, paroxysmal supraventricular tachycardia
50 J, atrial fibrillation 100 J, monomorphic ventricular
tachycardia100 J, polymorphic V tach 200 J.
Yes
Premedicate with midazolam (Versed) 25 mg IVP when
possible.
No or borderline
Atrial fibrillation
Atrial flutter
Paroxysmal
supraventricular
narrow complex
tachycardia
(PSVT)
Vagal maneuvers:
Carotid sinus
massage if no
bruits
Fig 6 Tachycardia
Adenosine
6 mg, rapid IV
push over 1-3 sec
1-2 min
Wide-complex
tachycardia of
uncertain type
Ventricular
tachycardia (VT)
If uncertain if V tach,
give Adenosine 6
mg rapid IV push
over 1-3 sec
1-2 min
Adenosine
12 mg, rapid IV
push over 1-3 sec
(may repeat once
in 1-2 min)
Torsade de pointes
(polymorphic VT)
Correct underlying
cause: Hypokal
emia, drug over
dose (tricyclic,
phenothiazine,
antiarrhythmic
class Ia, Ic, III)
Ad e no sine 12 m g , ra pid IV
p ush o ver 1 -3 se co nd s ( m ay
rep ea t o n ce in 1 -2 m in ); m a x
to ta l 30 m g
L id oca ine
1 -1 .5 m g/ kg IV pu sh .
R ep ea t 0.5 -0. 75
m g /kg IV P q 5-1 0m in
to m a x to ta l 3 m g/ kg
C om p lex wid th ?
W ide
N ar row
Blo od Pressure ?
Ve rap am il
2 .5-5 m g IV
1 5-30 m in
Ve rap am il
5 -1 0 m g I V
C on side r
D igo xin
Be ta b lo cke rs
D ilt iaze m
Ove rdr ive
p acing
Pr o cain am id e
2 0-30 m g /m in, m a x to ta l 1 7 m g /kg ;
fo llow ed b y 2 -4 m g /m in in fu sion
If W P W , a void a de no sine , b et a
b lo cke rs, ca lc iu m -blo cker s, an d
d ig oxin
F i g 6 - T a c h y c a r d ia
M ag ne sium 2-4 gm IV
o ver 5 -1 0 m in
Pro cain am id e 30
m g /m in IV to m ax
to ta l 17 m g /kg
STABLE TACHYCARDIA
Stable tachycardia with serious signs and
symptoms related to the tachycardia. Patient
not in cardiac arrest.
Synchronized cardioversion
Atrialflutter
50 J
PSVT
50 J
Atrial
100 J
Monomorphic V-tach 100 J
Polymorphic V tach 200 J
Fig 7 - Stable Tachycardia (not in cardiac arrest)
D e t e r m in e u n d e r ly in g c a u s e
A d m in is te r F lu id s, B lo o d
C o n s id e r v a s o p r e ss o r s
A p p ly h e m o s ta s is ; tr ea t
u n d e r ly in g p r o b le m
B ra d y c a r d i a o r T a c h y c a r d ia
P u m p F a i lu r e
H y p o v o l e m ia
D e ter m ine bl o o d p r es s u re
S y s toli c B P
< 70 m m H g
N o r e p in e p h r in e 0 . 5
3 0 : g / m in IV o r
D o p a m in e 5 -2 0 : g / kg
p e r m in
S y s t o li c B P
70- 10 0 m m H g
D o p a m in e 2 . 5 - 2 0
: g /k g p e r m in I V
( a d d n o r e p in e p h r in e
if d o p a m in e i s > 2 0
: g /k g p e r m in )
Systoli c B P >100 m m Hg
an d dia sto lic BP n orm al
D o b u t a m in e 2 .0 -2 0
: g / k g p e r m in I V
F u r o s e m id e IV 0 .5 -1.0 m g /kg
M or phi ne IV 1- 3 m g
N it r o g ly c e r in S L 0 .4 m g t a b
q 3 -5 m in x 3
O xy g e n
B ra d yc a r d ia T a c h y ca r d ia
G o t o F ig 5 G o to F ig 6
Diasto lic B P >11 0 mm Hg
I f is c h e m ia a n d h yp e rte n s io n :
N itr o g ly c e r in 1 0 -2 0 : g /m in
IV , an d titr a te to e ffec t a n d /o r
N itr o p r u s s id e 0 . 1 -5 .0
: g/k g / m in IV
Cardiac murmurs: 1/6 = faint; 2/6 = clear; 3/6 - loud; 4/6 = palpable; 5/6 = heard
Neuro
system.
therapy.
Infectious Disease: Plans for antibiotic therapy; antibiotic day number, culture
results.
Subjective: Patient is awake and alert. Note any events that occurred overnight.
ECG:
Chest x-ray:
Impression and Plan: Give an overall impression, and then discuss impression
Cardiovascular:
Pulmonary:
Neurological:
Gastrointestinal:
Infectious:
Endocrine:
Nutrition:
Procedure Note
A procedure note should be written in the chart when a procedure is performed.
Procedure notes are brief operative notes.
Procedure Note
18 Discharge Note
Procedure:
Indications:
the procedure were explained to the patient. Note that the patient was
given the opportunity to ask questions and that the patient consented to
Specimens: Describe any specimens obtained and labs tests which were
ordered.
ing staff.
Discharge Note
The discharge note should be written in the patients chart prior to discharge.
Discharge Note
Date/time:
Diagnoses:
Treatment: Briefly describe therapy provided during hospitalization,
including surgical procedures and antibiotic therapy.
Studies Performed: Electrocardiograms, CT scans.
Discharge medications:
Follow-up Arrangements:
500 mL
Dextrose 40-70%
500 mL
Sodium
35 mEq
Potassium
36 mEq
Chloride
35 mEq
Calcium
4.5 mEq
Phosphate
9 mMol
Magnesium
8.0 mEq
Acetate
82-104 mEq
20 Enteral Nutrition
Multi-Trace Element Formula
1 mL/d
Multivitamin 12 (2 amp)
10 mL/d
Vitamin B 12
1000 mcg/week
Fat Emulsion:
-Intralipid 20% 500 mL/d IVPB infused in parallel with standard solution at 1
mL/min x 15 min; if no adverse reactions, increase to 20-50 mL/hr. Serum
triglyceride level should be checked 6h after end of infusion (maintain
<250 mg/dL).
Cyclic Total Parenteral Nutrition
-12-hour night schedule; taper continuous infusion in morning by reducing rate
to half original rate for 1 hour. Further reduce rate by half for an additional
hour, then discontinue. Restart TPN in evening. Taper at beginning and
end of cycle. Final rate should be 185 mL/hr for 9-10h with 2 hours of
taper at each end, for total of 2000 mL.
Peripheral Parenteral Supplementation
-Amino acid solution (ProCalamine) 3% up to 3 L/d at 125 cc/h OR
-Combine 500 mL amino acid solution 7% or 10% (Aminosyn) and 500 mL
20% dextrose and electrolyte additive. Infuse at up to 100 cc/hr in
parallel with intralipid 10% or 20% at 1 mL/min for 15 min (test dose);
if no adverse reactions, infuse 500 mL/d at 20 mL/hr.
Special Medications
-Famotidine (Pepcid) 20 mg IV q12h or 40 mg/day in TPN OR
-Ranitidine (Zantac) 50 mg IV q6-8h.
-Insulin sliding scale or continuous IV infusion.
Labs
Baseline: Draw labs below. Chest x-ray, plain film for tube placement
Daily Labs: Chem 7, osmolality, CBC, cholesterol, triglyceride (6h after end
of infusion), serum phosphate, magnesium, calcium, urine specific gravity.
Weekly Labs: Protein, iron, TIBC, INR/PTT, 24h urine nitrogen and
creatinine. Pre-albumin, transferrin, albumin, total protein, AST, ALT,
GGT, alkaline phosphatase, LDH, amylase, total bilirubin.
Enteral Nutrition
General Measures: Daily weights, nasoduodenal feeding tube. Head of bed at
30 degrees while enteral feeding and 2 hours after completion. Record bowel
movements.
Continuous Enteral Infusion: Initial enteral solution (Osmolite, Pulmocare,
Jevity) 30 mL/hr. Measure residual volume q1h x 12h, then tid; hold feeding
for 1 h if residual is more than 100 mL of residual. Increase rate by 25-50
mL/hr at 24 hr intervals as tolerated until final rate of 50-100 mL/hr (1 cal/mL)
as tolerated. Three tablespoons of protein powder (Promix) may be added to
each 500 cc of solution. Flush tube with 100 cc water q8h.
Enteral Bolus Feeding: Give 50-100 mL of enteral solution (Osmolite,
Pulmocare, Jevity) q3h initially. Increase amount in 50 mL steps to max of
250-300 mL q3-4h; 30 kcal of nonprotein calories/d and 1.5 gm protein/kg/d.
Before each feeding measure residual volume, and delay feeding by 1 h if
>100 mL. Flush tube with 100 cc of water after each bolus.
Special Medications:
Symptomatic Medications:
-Loperamide (Imodium) 24 mg PO or in J-tube q6h, max 16 mg/d prn OR
-Diphenoxylate/atropine (Lomotil) 5-10 mL (2.5 mg/5 mL) PO or in J-tube q4
6h, max 12 tabs/d OR
-Kaopectate 30 cc PO or in J-tube q6h.
1-7 mm Hg
15-25 mm Hg
8-15 mm Hg
15-25 mm Hg
8-15 mm Hg
10-20 mm Hg
Cardiovascular Disorders
Roham T. Zamanian, MD
Farhad Mazdisnian, MD
Michael Krutzik, MD
Initial Eleva
tion After MI
Mean Time to
Peak Eleva
tions
Time to Re
turn to Base
line
Myoglobin
1-4 h
6-7 h
18-24 h
CTnl
3-12 h
10-24 h
3-10 d
CTnT
3-12 h
12-48 h
5-14 d
CKMB
4-12 h
10-24 h
48-72 h
CKMBiso
2-6 h
12 h
38 h
Exclusion
Recommendation
Thrombolytics:
Inclusion
Exclusion
Recommendation
Heparin:
Inclusion
Exclusion
Recommendation
Beta-Blockade:
Inclusion
Exclusion
Recommendation
Nitrates:
Inclusion
Exclusion
Recommendation
ACE Inhibitors:
Inclusion
Exclusion
Recommendation
C. Thrombolytics
1. ECG criteria for thrombolysis
a. ST Elevation (>1 mm in two or more contiguous leads), time to
therapy 12 hours or less, age younger than 75 years.
b. A new bundle branch block (obscuring ST-segment analysis) and
history suggesting acute MI.
2. Alteplase (t-PA, tissue-plasminogen activator, Activase) and
Reteplase (Retavase) convert plasminogen to plasmin. Both agents
are clot-specific and bind to new thrombus. Activase is superior to
streptokinase. The alteplase thirty-day mortality rate of 6.3% is the
lowest of the fibrinolytics, compared with 7.3% for streptokinase.
Alteplase provides the earliest and most complete reperfusion.
3. Streptokinase (SK, Streptase) provides greater benefit in older
patients with a smaller amount of myocardium at risk who present
later and those with a greater risk of ICH. The dose of IV SK is 1.5
million units given over 60 minutes.
D. Reperfusion therapy: Percutaneous coronary intervention
Heart Failure 33
A. Patients with a nondiagnostic ECG who have an indeterminate or a low
risk of MI should receive aspirin while undergoing serial cardiac enzyme
studies and repeat ECGs.
B. Treadmill stress testing should be considered for patients with a
suspicion of coronary ischemia.
Heart Failure
Congestive heart failure (CHF) is defined as the inability of the heart to meet the
metabolic and nutritional demands of the body. Approximately 75% of patients
with heart failure are older than 65-70 years of age. Approximately 8% of patients
between the ages of 75 and 86 have heart failure.
I. Etiology
A. The most common causes of CHF are coronary artery disease, hyperten
sion, and alcoholic cardiomyopathy. Valvular diseases such as aortic
stenosis and mitral regurgitation, are also common.
B. Coronary artery disease is the etiology of heart failure in two-thirds of
patients with left ventricular dysfunction. Heart failure should be presumed
to be of ischemic origin until proven otherwise.
II. Clinical presentation
A. Left heart failure produces dyspnea and fatigue. Right heart failure leads
to lower extremity edema, ascites, congestive hepatomegaly, and jugular
venous distension. Symptoms of pulmonary congestion include dyspnea,
orthopnea, and paroxysmal nocturnal dyspnea. Clinical impairment is
caused by left ventricular systolic dysfunction (ejection fraction of less than
40%) in 80-90% of patients with CHF.
B. Patients should be evaluated for coronary artery disease, hypertension,
and valvular dysfunction. Use of alcohol, chemotherapeutic agents
(daunorubicin), negative inotropic agents, and symptoms of a recent viral
syndrome should be assessed.
C. CHF can present with shortness of breath, dyspnea on exertion, paroxys
mal nocturnal dyspnea, orthopnea, nocturia, and cough. Exertional
dyspnea is extremely common in patients with heart failure.
Precipitants of Congestive Heart Failure
Myocardial ischemia or infarc
tion
Atrial fibrillation
Worsening valvular disease
Pulmonary embolism
Hypoxia
Severe, uncontrolled hyperten
sion
Thyroid disease
Pregnancy
Anemia
Infection
Tachycardia or bradycardia
Alcohol abuse
Medication or dietary noncompli
ance
34 Heart Failure
apical impulse. Poor capillary refill, cool extremities, or an altered level of
consciousness may also be present.
New York Heart Association Criteria for Heart Failure
Class I
Class II
Class III
Class IV
Asymptomatic
Symptoms with moderate activity
Symptoms with minimal activity
Symptoms at rest
E. Laboratory assessment
1. Patients with symptoms suggestive of CHF should have a 12-lead
ECG.
2. Impedance cardiography (ICG) is a noninvasive, reliable method of
measuring cardiac index and stroke volume. It should be done on the
first day of hospitalization and repeated to assess response to drug
therapy.
3. A chest x-ray should be performed to identify pleural effusions,
pneumothorax, pulmonary edema, or infiltrates.
4. If cardiac ischemia or infarction is suspected, cardiac enzymes should
be drawn. A complete blood count, electrolytes, and digoxin level, if
applicable, also are mandatory. Patients with suspected hyper
thyroidism should have thyroid function studies drawn.
F. Echocardiography is recommended to evaluate the presence of
pericardial effusion, tamponade, valvular regurgitation, wall motion
abnormalities, and ejection fraction.
Laboratory Workup for Suspected Heart Failure
Blood urea nitrogen
Cardiac enzymes (CK-MB,
troponin, or both)
Complete blood cell count
Creatinine
Electrolytes
Liver function tests
III.
Magnesium
Thyroid-stimulating hormone
Urinalysis
Echocardiogram
Electrocardiography
Impedance cardiography
Heart Failure 35
36 Heart Failure
slowly. Beta-blockers should not be used in acute pulmonary edema or
decompensated heart failure, and they should only be initiated in the
stable patient. Beta-blockers are an add-on therapy for patients being
treated with ACE inhibitors.
Carvedilol, Metoprolol, and Bisoprolol Dosages and Side Effects
Carvedilol (Coreg) start at 1.625-3.125 mg bid; target dose 25-50 mg
bid
Metoprolol (Lopressor) start at 12.5 mg bid; target dose 100 mg bid
Bisoprolol (Zebeta) start at 1.25 mg qd; target dose 10 mg qd
Digoxin Dosing
Start at 0.250 mg/d with near normal renal function; start at 0.125 mg/d
if renal function impaired.
Maintain serum digoxin level of 0.8-1.2 ng/mL.
G. Digoxin does not improve survival in CHF (as do ACE-inhibitors and
beta-blockers). Digoxin may be added to a regimen of ACE-inhibitors and
diuretics if symptoms of heart failure persist. Digoxin can increase
exercise tolerance, improve symptoms, and decrease the risk of
hospitalization.
H. Spironolactone improves mortality in severe CHF and should be used
in addition to an ACE-inhibitor or ARB. A dosage of 25 mg qd should be
considered in patients with severe CHF. It can cause hyperkalemia, rash,
and gynecomastia.
I. Nonpharmacologic treatments
1. Salt restriction (a diet with 2 g sodium or less), alcohol restriction,
water restriction for patients with severe renal impairment, and regular
aerobic exercise as tolerated.
2. Synchronized biventricular pacing in patients with an ejection fraction
of <40% and wide QRS duration of >150 msec may improve symp
toms and the overall clinical course.
J. Inotropic support
1. Positive inotropic agents improve quality of life and reduce need for
hospitalization but increase mortality. Parenterally positive inotropic
therapy increases cardiac output and decreases symptoms of
congestion.
2. Parenteral inotropic agents can be administered continuously in
patients with exacerbations of heart failure. These agents may be
administered continuously or intermittently at home. Impedance
cardiography is used to assess clinical response before and during
treatment.
Atrial Fibrillation 37
Atrial Fibrillation
Atrial fibrillation (AF) is the most common arrhythmia. The median age of onset
is 75, and the incidence and prevalence increase dramatically with age. For
patients older than 80 years, the incidence of AF is 9%. For patients aged 80-90,
nearly one-third of strokes that occur are related to AF.
I. Pathophysiology. The cardiac conditions most commonly associated with
AF are coronary artery disease, hypertension, rheumatic heart disease, mitral
valve disease, cardiomyopathies, and open-heart surgery. Hypertension and
coronary artery disease are the most frequent risk factors, accounting for 65%
of AF cases. The most common noncardiac causes are pulmonary diseases
(including COPD), hypoxia, and hyperthyroidism.
II. Clinical evaluation
38 Atrial Fibrillation
A. Patients with AF often experience dyspnea and palpitations, although
some may be asymptomatic. AF may be associated with palpitations,
dizziness, dyspnea, chest pain, syncope, fatigue, or confusion.
B. The most common physical sign of AF is an irregular pulse. Other
physical exam findings include a pulse deficit, absent a wave in the
jugular venous pulse, and a variable intensity of the first heart sound.
Causes of Atrial Fibrillation
Structural Heart Disease
Hypertension
Ischemic heart disease
Valvular heart disease: Mitral stenosis,
aortic stenosis, mitral regurgitation
Pericarditis
Cardiac tumors
Sick sinus syndrome
Cardiomyopathies
Congenital heart disease
Wolf-Parkinson-White syndrome
Atrial Fibrillation 39
younger than 65 and without these risk factors (lone AF), aspirin
alone may be appropriate for stroke prevention.
4. Patients between the ages of 65 and 75 with none of these risk
factors could be treated with either warfarin or aspirin.
5. In patients older than 75 with AF, oral anticoagulation with warfarin is
recommended. In patients with major contraindications to warfarin
(intracranial hemorrhage, unstable gait, falls, syncope, or poor
compliance), a daily aspirin is a reasonable alternative.
6. If the duration of AF is unknown or more than 48 hours, then rate
control and anticoagulation therapy should be initiated first. The
patient should be evaluated for the presence of an intracardiac
thrombus with a transesophageal echocardiography (TEE). If the TEE
demonstrates a clot, the patient is anticoagulated for three weeks
before a scheduled cardioversion. If no left atrial thrombus is
identified by TEE, heparin is started and the patient is cardioverted.
Following successful cardioversion, the patient is placed on warfarin
for an additional four weeks.
C. Rate control
1. Patients with AF of greater than one year duration or a left atrial size
greater than 50 mm may have difficulty in converting to sinus rhythm.
In these patients, rate control, rather than conversion to sinus rhythm
may, be beneficial. A controlled ventricular rate in AF is less than 90
bpm at rest.
2. The pharmacological agents used for rate control are calcium channel
blockers (diltiazem, verapamil), beta-blockers (metoprolol, esmolol)
and digoxin. Calcium channel blockers should be used first because
of rapid onset of action compared to digoxin, which takes 4-6 hours
to show pharmacological effect. Digoxin is the first drug of choice in
significant left ventricular dysfunction.
3. Calcium channel blockers can slow AV node conduction and are
first-line agents for rate control therapy.
4. Beta-blockers slow AV nodal and sinoatrial nodal conduction. The
most commonly used beta-blockers are metoprolol and atenolol.
5. Digoxin has numerous drug interactions, an unpredictable dose
response curve, and a potentially lethal toxicity. Digoxin is is reserved
for patients with systolic dysfunction and heart failure.
Agents Used for Heart Rate Control in Atrial Fibrillation
Agent
Loading
Dose
Onset of Ac
tion
Maintenance
Dosage
Major Side
Effects
Diltiazem
(Cardizem)
0.25 mg per
kg IV over 2
minutes, may
repeat dose
with 0.35
mg/kg after 15
min x 1
2-7 minutes
5-15 mg per
hour IV or 120
360 mg PO ev
ery day in div
ided doses
Hypotension,
heart block,
heart failure
Verapamil
(Calan,
Isoptin)
0.075-0.15 mg
per kg IV over
2 minutes
3-5 minutes
240-360 mg PO
every day in
divided doses
Hypotension,
heart block,
heart failure
40 Atrial Fibrillation
Agent
Loading
Dose
Onset of Ac
tion
Maintenance
Dosage
Major Side
Effects
Esmolol
(Brevibloc)
0.5 mg per kg
IV over one
minute
5 minutes
0.05-0.2
mg/kg/minute
IV
Hypotension,
heart block,
bradycardia,
asthma, heart
failure
Metoprolol
(Lopressor)
2.5-5 mg IV
bolus over 2
minutes, up to
3 doses
5 minutes
50-200 mg PO
every day in 2
daily doses
Hypotension,
heart block,
bradycardia,
asthma, heart
failure
Propranolol
(Inderal)
0.15 mg per
kg
5 minutes
40-320 mg PO
every day in
divided doses
Hypotension,
heart block,
bradycardia,
asthma, heart
failure
Digoxin
(Lanoxin)
0.25 mg IV or
PO every 4
hours, up to
1.0-1.5 mg
4-6 hours
0.125-0.25 mg
PO/IV qd
Digitalis toxic
ity, heart
block, brady
cardia, ven
tricular fibrilla
tion
Mechanism
of Action
ECG
Changes
Dose
Adverse Re
action
QRS wid
ens, QT
lengthens
Sulfate 300-600
mg po q6-8hrs
Quinaglute 324
628 mg po q8
12 hrs
GI, cinchonism
VT/VF/
Torsade de
Pointes
QRS wid
ens, QT
lengthens
Load: IV 13-17
mg/kg over 30
60 min
Maintenance: IV
2-4 mg/min or
Procan SR 750
1500 mg po
q6hr
SLE-like syn
drome, confu
sion
Class la Agents
Quinidine
Procain
amide
Decrease Na
influx
Reduce
upstroke
velocity,
Prolong
repolariza
tion
Atrial Fibrillation 41
Class Ic Agents
Flecainide
Reduction in
upstroke
velocity
Propa
fenone
QRS wid
ens, QT
lengthens
Start 50-100 mg
po q12hr; max.
200 bid
Dizziness,
headaches
QRS wid
ens, QT
lengthens
Start 150 mg po
q8hrs; max. 300
mg po q8hr
Dose
depend
ant QT
prolonga
tion
Load 400 mg po
tid x 7-14 days,
then 400 mg po
qd x 1 month;
Maintenance:
100-400 mg/day
Ataxia, trem
ors pulmonary
fibrosis, pneu
mon
itis/alveolitis,
skin discolor
ation, thyroid
and LFT
abnormalities
Amio
darone
Blocks K
efflux, pro
longs
repolar
ization
Sotalol
Potent beta
blocking ac
tivity
80 mg po bid;
max. 160 mg bid
Bradycardia,
Torsade de
Pointes.
Ibutilide
Prolong ac
tion potential
and refrac
tory period
1 mg IV infusion
over 10 min,
may repeat once
after 10 min
Torsade in 3
8%
125-500 mcg
bid, depending
on renal function
0.5-10% tor
sade
Dofetilide
42 Hypertensive Emergency
heart disease. It is reserved for patients with normal LV function
and refractory AF.
b. Propafenone may have fewer side effects and is better tolerated
than the Ia agents. It is available only in an oral form and can also
be given as a single bolus dose for AF of less than 24 hours.
Proarrhythmia can occur but is reported less frequently than with
the other Ic medications. Propafenone is useful for patients who
are hypertensive and have a structurally normal heart with AF.
Propafenone should be avoided in patients with structural heart
disease.
3. Class III. The medications in this class act by blocking outward
potassium currents, resulting in increased myocardial refractoriness.
All class III agents cause a dose-dependent QTc prolongation,
resulting in Torsades de Pointes. These agents are contraindicated
if the QTc is >0.44 seconds.
a. Amiodarone (Cordarone) has sodium, calcium, and beta
blocking effects. Amiodarone has a low proarrhythmia profile. It is
safe and efficacious in patients with CHF and AF. Side effects
include pulmonary fibrosis, pneumonitis, skin discoloration, thyroid
and liver abnormalities, ataxia, and tremors (33%).
b. Sotalol (Betapace) has a beta-blocking effect. It is less effective
than quinidine, with a conversion rate of 20%. It is most appropri
ate for sinus maintenance in patients with AF and coronary artery
disease. Sotalol should be avoided in patients with severe LV
dysfunction and COPD.
c. Ibutilide (Corvert) is highly effective for the conversion of recent
onset AF (30%) and atrial flutter (70%). Polymorphic ventricular
tachycardia occurs in about 6%. Pretreatment with magnesium
may prevent polymorphic ventricular tachycardia.
d. Dofetilide (Tikosyn) is indicated for acute conversion and
maintenance of atrial fibrillation. The success rate in acute
conversion is 30%.
E. Nonpharmacologic strategies. Due to drug intolerance, possible
proarrhythmic effects, and disappointing long-term efficacy of the
antiarrhythmic agents, non-pharmacological therapies have an important
role in the management of AF.
1. Electrical cardioversion is rapid and highly effective, with success
rates greater than 80%.
2. Radiofrequency catheter ablation/atrial defibrillators. The
delivery of radiofrequency current through a catheter tip advanced to
the atrium is highly effective and safe.
Hypertensive Emergency
Hypertensive crises are severe elevations in blood pressure (BP) characterized
by a diastolic blood pressure (BP) higher than 120-130 mm Hg.
I. Clinical evaluation of hypertensive crises
A. Hypertensive emergency is defined by a diastolic blood pressure >120
mm Hg associated with ongoing vascular damage. Symptoms or signs of
Hypertensive Emergency 43
neurologic, cardiac, renal, or retinal dysfunction are present. Hypertensive
emergencies include severe hypertension in the following settings:
1. Aortic dissection
2. Acute left ventricular failure and pulmonary edema
3. Acute renal failure or worsening of chronic renal failure
4. Hypertensive encephalopathy
5. Focal neurologic damage indicating thrombotic or hemorrhagic stroke
6. Pheochromocytoma, cocaine overdose, or other hyperadrenergic
states
7. Unstable angina or myocardial infarction
8. Eclampsia
B. Hypertensive urgency is defined as diastolic blood pressure >120 mm
Hg without evidence of vascular damage; the disorder is asymptomatic
and no retinal lesions are present.
C. Causes of secondary hypertension include renovascular hypertension,
pheochromocytoma, cocaine use, withdrawal from alpha-2 stimulants,
clonidine, beta-blockers or alcohol, and noncompliance with
antihypertensive medications.
44 Hypertensive Emergency
II. Initial assessment of severe hypertension
A. When severe hypertension is noted, the measurement should be repeated
in both arms to detect any significant differences. Peripheral pulses should
be assessed for absence or delay, which suggests dissecting aortic
dissection. Evidence of pulmonary edema should be sought.
B. Target organ damage is suggested by chest pain, neurologic signs,
altered mental status, profound headache, dyspnea, abdominal pain,
hematuria, focal neurologic signs (paralysis or paresthesia), or hyperten
sive retinopathy.
C. Prescription drug use should be assessed, including missed doses of
antihypertensives. History of recent cocaine or amphetamine use should
be sought.
D. If focal neurologic signs are present, a CT scan may be required to
differentiate hypertensive encephalopathy from a stroke syndrome.
III. Laboratory evaluation
A. Complete blood cell count, urinalysis for protein, glucose, and blood; urine
sediment examination; chemistry panel (SMA-18).
B. If chest pain is present, cardiac enzymes are obtained.
C. If the history suggests a hyperadrenergic state, the possibility of a
pheochromocytoma should be excluded with a 24-hour urine for catechol
amines. A urine drug screen may be necessary to exclude illicit drug use.
D. Electrocardiogram should be completed.
E. Suspected primary aldosteronism can be excluded with a 24-hour urine
potassium and an assessment of plasma renin activity. Renal artery
stenosis can be excluded with captopril renography and intravenous
pyelography.
Screening Tests for Secondary Hypertension
Renovascular Hyper
tension
Hyperaldosteronism
Serum potassium
24-hr urine potassium
Plasma renin activity
CT scan of adrenals
Pheochromocytoma
Cushing's Syndrome
Plasma ACTH
Dexamethasone suppression test
Hyperparathyroidism
Serum calcium
Serum parathyroid hormone
Hypertensive Emergency 45
Rapid, uncontrolled reductions in blood pressure should be avoided
because coma, stroke, myocardial infarction, acute renal failure, or death
may result.
B. The goal of initial therapy is to terminate ongoing target organ damage.
The mean arterial pressure should be lowered not more than 20-25%, or
to a diastolic blood pressure of 100 mm Hg over 15 to 30 minutes.
V. Parenteral antihypertensive agents
A. Nitroprusside (Nipride)
1. Nitroprusside is the drug of choice in almost all hypertensive emergen
cies (except myocardial ischemia or renal impairment). It dilates both
arteries and veins, and it reduces afterload and preload. Onset of
action is nearly instantaneous, and the effects disappear 1-2 minutes
after discontinuation.
2. The starting dosage is 0.25-0.5 mcg/kg/min by continuous infusion
with a range of 0.25-8.0 mcg/kg/min. Titrate dose to gradually reduce
blood pressure over minutes to hours.
3. When treatment is prolonged or when renal insufficiency is present,
the risk of cyanide and thiocyanate toxicity is increased. Signs of
thiocyanate toxicity include anorexia, disorientation, fatigue, hallucina
tions, nausea, toxic psychosis, and seizures.
B. Nitroglycerin
1. Nitroglycerin is the drug of choice for hypertensive emergencies with
coronary ischemia. It should not be used with hypertensive
encephalopathy because it increases intracranial pressure.
2. Nitroglycerin increases venous capacitance, decreases venous return
and left ventricular filling pressure. It has a rapid onset of action of 2-5
minutes. Tolerance may occur within 24-48 hours.
3. The starting dose is 15 mcg IV bolus, then 5-10 mcg/min (50 mg in
250 mL D5W). Titrate by increasing the dose at 3- to 5-minute inter
vals up to max 1.0 mcg/kg/min.
C. Labetalol IV (Normodyne)
1. Labetalol is a good choice if BP elevation is associated with
hyperadrenergic activity, aortic dissection, an aneurysm, or post
operative hypertension.
2. Labetalol is administered as 20 mg slow IV over 2 min. Additional
doses of 20-80 mg may be administered q5-10min, then q3-4h prn or
0.5-2.0 mg/min IV infusion. Labetalol is contraindicated in obstructive
pulmonary disease, CHF, or heart block greater than first degree.
D. Enalaprilat IV (Vasotec)
1. Enalaprilat is an ACE-inhibitor with a rapid onset of action (15 min) and
long duration of action (11 hours). It is ideal for patients with heart
failure or accelerated-malignant hypertension.
2. Initial dose, 1.25 mg IVP (over 2-5 min) q6h, then increase up to 5 mg
q6h. Reduce dose in azotemic patients. Contraindicated in bilateral
renal artery stenosis.
E. Esmolol (Brevibloc) is a non-selective beta-blocker with a 1-2 min onset
of action and short duration of 10 min. The dose is 500 mcg/kg/min x 1
min, then 50 mcg/kg/min; max 300 mcg/kg/min IV infusion.
F. Hydralazine is a preload and afterload reducing agent. It is ideal in
hypertension due to eclampsia. Reflex tachycardia is common. The dose
is 20 mg IV/IM q4-6h.
46 Ventricular Arrhythmias
G.
Ventricular Arrhythmias
I. Ventricular fibrillation and tachycardia
-If unstable (see ACLS protocol page 5), defibrillate with unsynchronized
200 J, 300 J, then 360 J.
-Oxygen 100% by mask.
-Procainamide loading dose 10-15 mg/kg at 20 mg/min IV or 100 mg IV
q10min, then 2-4 mg/min IV maintenance OR
-Also see other antiarrhythmics below.
II. Torsades de Pointes
-Correct underlying cause and consider discontinuing drugs that cause
Torsades de Pointes (dofetilide, ibutilide, sotalol, amiodarone, quinidine,
procainamide, disopyramide, moricizine, bepridil, phenothiazines, tricyclic
and tetracyclic antidepressants, vasopressin, imidazoles, pentamidine);
correct hypokalemia and hypomagnesemia.
-Defibrillate with 360 J.
Acute Pericarditis
Pericarditis is the most common disease of the pericardium. The most common
cause of pericarditis is viral infection. This disorder is characterized by chest
pain, a pericardial friction rub, electrocardiographic changes, and pericardial
effusion.
I. Clinical features
A. Chest pain of acute infectious (viral) pericarditis typically develops in
younger adults 1 to 2 weeks after a viral illness. The chest pain is of
sudden and severe onset, with retrosternal and/or left precordial pain and
referral to the back and trapezius ridge. Pain may be preceded by low
grade fever. Radiation to the arms may also occur. The pain is often
pleuritic (eg, accentuated by inspiration or coughing) and may also be
relieved by changes in posture (upright posture).
B. A pericardial friction rub is the most important physical sign. It is often
described as triphasic, with systolic and both early (passive ventricular
filling) and late (atrial systole) diastolic components, or more commonly
a biphasic (systole and diastole).
C. Resting tachycardia (rarely atrial fibrillation) and a low-grade fever may be
present.
Causes of Pericarditis
Idiopathic
Infectious: Viral, bacterial, tubercu
lous, parasitic, fungal
Connective tissue diseases Meta
bolic: uremia, hypothyroidism Neo
plasm, radiation
II.
Hypersensitivity: drug
Postmyocardial injury syndrome
Trauma
Dissecting aneurysm
Chylopericardium
Diagnostic testing
A. ECG changes. During the initial few days, diffuse (limb leads and
precordial leads) ST segment elevations are common in the absence of
reciprocal ST segment depression. PR segment depression is also
common and reflects atrial involvement.
B. The chest radiograph is often unrevealing, although a small left pleural
effusion may be seen. An elevated erythrocyte sedimentation rate and
C-reactive protein (CRP) and mild elevations of the white blood cell
count are also common.
C. Labs: CBC, SMA 12, albumin, viral serologies: Coxsackie A & B,
measles, mumps, influenza, ASO titer, hepatitis surface antigen, ANA,
rheumatoid factor, anti-myocardial antibody, PPD with candida, mumps.
Cardiac enzymes q8h x 4, ESR, blood C&S X 2.
D. Pericardiocentesis: Gram stain, C&S, cell count & differential,
cytology, glucose, protein, LDH, amylase, triglyceride, AFB, specific
gravity, pH.
48 Pacemakers
E. Echocardiography is the most sensitive test for detecting pericardial
effusion, which may occur with pericarditis.
III. Treatment of acute pericarditis (nonpurulent)
A. If effusion present on echocardiography, pericardiocentesis should be
performed and the catheter should be left in place for drainage.
B. Treatment of pain starts with nonsteroidal anti-inflammatory drugs,
meperidine, or morphine. In some instances, corticosteroids may be
required to suppress inflammation and pain.
C. Anti-inflammatory treatment with NSAIDs is first-line therapy.
1. Indomethacin (Indocin) 25 mg tid or 75 mg SR qd, OR
2. Ketorolac (Toradol) 15-30 mg IV q6h, OR
3. Ibuprofen (Motrin) 600 mg q8h.
D. Morphine sulfate 5-15 mg intramuscularly every 4-6 hours. Meperidine
(Demerol) may also be used, 50-100 mg IM/IV q4-6h prn pain and
promethazine (Phenergan) 25-75 mg IV q4h.
E. Prednisone, 60 mg daily, to be reduced every few days to 40, 20, 10,
and 5 mg daily.
F. Purulent pericarditis
1. Nafcillin or oxacillin 2 gm IV q4h AND EITHER
2. Gentamicin or tobramycin 100-120 mg IV (1.5-2 mg/kg); then 80 mg
(1.0-1.5 mg/kg) IV q8h (adjust in renal failure) OR
3. Ceftizoxime (Cefizox) 1-2 gm IV q8h.
4. Vancomycin, 1 gm IV q12h, may be used in place of nafcillin or
oxacillin.
Pacemakers
Indications for implantation of a permanent pacemaker are based on symptoms,
the presence of heart disease and the presence of symptomatic
bradyarrhythmias. Pacemakers are categorized by a three- to five-letter code
according to the site of the pacing electrode and the mode of pacing.
I. Indications for pacemakers
A. First-degree atrioventricular (AV) block can be associated with severe
symptoms. Pacing may benefit patients with a PR interval greater than
0.3 seconds. Type I second-degree AV block does not usually require
permanent pacing because progression to a higher degree AV block is
not common. Permanent pacing improves survival in patients with
complete heart block.
B. Permanent pacing is not needed in reversible causes of AV block, such
as electrolyte disturbances or Lyme disease. Implantation is easier and
of lower cost with single-chamber ventricular demand (VVI) pacemakers,
but use of these devices is becoming less common with the advent of
dual-chamber demand (DDD) pacemakers.
Pacemakers 49
Position 2
(chamber
sensed)
Position 3
(response to
sensing)
Position 4
(programma
ble functions;
rate modula
tion)
Position 5
(antitachy
arrhythmia
functions)
V--ventricle
V--ventricle
T--triggered
P--program
mable rate
and/or output
P--pacing
(antitachy
arrhythmia)
A--atrium
A--atrium
I--inhibited
M--multipro
grammability
of rate, output,
sensitivity, etc.
S--shock
D--dual (A
& V)
D--dual (A
& V)
D--dual (T &
I)
C--communi
cating (telem
etry)
D--dual (P +
S)
O--none
O--none
O--none
R--rate modu
lation
O--none
O--none
C. Sick sinus syndrome (or sinus node dysfunction) is the most common
reason for permanent pacing. Symptoms are related to the
bradyarrhythmias of sick sinus syndrome. VVI mode is typically used in
patients with sick sinus syndrome, but recent studies have shown that
DDD pacing improves morbidity, mortality and quality of life.
II. Temporary pacemakers
A. Temporary pacemaker leads generally are inserted percutaneously, then
positioned in the right ventricular apex and attached to an external
generator. Temporary pacing is used to stabilize patients awaiting
permanent pacemaker implantation, to correct a transient symptomatic
bradycardia due to drug toxicity or to suppress Torsades de Pointes by
maintaining a rate of 85-100 beats per minute until the cause has been
eliminated.
B. Temporary pacing may also be used in a prophylactic fashion in patients
at risk of symptomatic bradycardia during a surgical procedure or high
degree AV block in the setting of an acute myocardial infarction.
C. In emergent situations, ventricular pacing can be instituted immediately
by transcutaneous pacing using electrode pads applied to the chest wall.
References
ACC/AHA Guidelines for Management of Patients with Acute Myocardial Infarction.
Circulation 1999; 100; 1016-1030.
ACC/AHA Guidelines for Management of Patients with Unstable Angina and NonSTSegment Elevation Myocardial Infarction. Circulation 2000; 102; 1193-1209.
Acute Coronary Syndromes (Acute Myocardial Infarction). Circulation 2000; 102 (supp I):
I172-I203.
50 Pacemakers
Consensus recommendations for the management of chronic heart failure. Am J Card (supp)
Jan 21, 1999.
Bristow MR, et al: Heart failure management using implantable devices for ventricular
resynchronization: Companion Trial. J of Cardiac Failure, 2000: 6; 276-284.
Yeghiazarians, Y. et al: Unstable Angina Pectoris: NEJM 2000; 342 #2; 101-112.
Wright, RS et al: Update on Intravenous Fibrinolytic Therapy for Acute Myocardial Infarction.
Mayo Clin Proc 2000; 75:1185-92.
Adams, et al. Heart Failure Society Guidelines. Pharmacotherapy 2000; 20 (5): 496-520
Skrabal, et al. Advances in the Treatment of CHF: New Approaches for an Old Disease.
Pharmacotherapy 2000; 20 (7): 787-804.
Orotracheal Intubation 51
Pulmonary Disorders
T. Scott Gallacher, MD
Ryan Klein, MD
Michael Krutzik, MD
Thomas Vovan, MD
Orotracheal Intubation
Endotracheal Tube Size (interior diameter):
Women 7.0-9.0 mm
Men 8.0-10.0 mm
1. Prepare suction apparatus. Have Ambu bag and mask apparatus setup with
100% oxygen; and ensure that patient can be adequately bag ventilated and
suction apparatus is available.
2. If sedation and/or paralysis is required, consider rapid sequence induction as
follows:
A. Fentanyl (Sublimaze) 50 mcg increments IV (1 mcg/kg) with:
B. Midazolam (Versed) 1 mg IV q2-3 min. max 0.1-0.15 mg/kg followed by:
C. Succinylcholine (Anectine) 0.6-1.0 mg/kg, at appropriate intervals; or
vecuronium (Norcuron) 0.1 mg/kg IV x 1.
D. Propofol (Diprivan): 0.5 mg/kg IV bolus.
E. Etomidate (Amidate): 0.3-0.4 mg/kg IV.
3. Position the patient's head in the sniffing position with head flexed at neck
and extended. If necessary, elevate the head with a small pillow.
4. Ventilate the patient with bag mask apparatus and hyperoxygenate with
100% oxygen.
5. Hold laryngoscope handle with left hand, and use right hand to open the
patients mouth. Insert blade along the right side of mouth to the base of
tongue, and push the tongue to the left. If using curved blade, advance it to
the vallecula (superior to epiglottis), and lift anteriorly, being careful not to
exert pressure on the teeth. If using a straight blade, place beneath the
epiglottis and lift anteriorly.
6. Place endotracheal tube (ETT) into right corner of mouth and pass it through
the vocal cords; stop just after the cuff disappears behind vocal cords. If
unsuccessful after 30 seconds, stop and resume bag and mask ventilation
before re-attempting. A stilette to maintain the shape of the ETT in a hockey
stick shape may be used. Remove stilette after intubation.
7. Inflate cuff with syringe keeping cuff pressure <20 cm H2O, and attach the
tube to an Ambu bag or ventilator. Confirm bilateral, equal expansion of the
chest and equal bilateral breath sounds. Auscultate the abdomen to confirm
that the ETT is not in the esophagus. If there is any question about proper
ETT location, repeat laryngoscopy with tube in place to be sure it is
endotracheal. Remove the tube immediately if there is any doubt about
proper location. Secure the tube with tape and note centimeter mark at the
mouth. Suction the oropharynx and trachea.
8. Confirm proper tube placement with a chest x-ray (tip of ETT should be
between the carina and thoracic inlet, or level with the top of the aortic
notch).
52 Nasotracheal Intubation
Nasotracheal Intubation
Nasotracheal intubation is the preferred method of intubation if prolonged
intubation is anticipated (increased patient comfort). Intubation will be facilitated
if the patient is awake and spontaneously breathing. There is an increased
incidence of sinusitis with nasotracheal intubation.
1. Spray the nasal passage with a vasoconstrictor such as cocaine 4% or
phenylephrine 0.25% (Neo-Synephrine). If sedation is required before
nasotracheal intubation, administer midazolam (Versed) 0.05-0.1 mg/kg IV
push. Lubricate the nasal airway with lidocaine ointment.
Tube Size:
Women 7.0 mm tube
Men 8.0, 9.0 mm tube
2. Place the nasotracheal tube into the nasal passage, and guide it into
nasopharynx along a U-shaped path. Monitor breath sounds by listening and
feeling the end of tube. As the tube enters the oropharynx, gradually guide the
tube downward. If the breath sounds stop, withdraw the tube 1-2 cm until
breath sounds are heard again. Reposition the tube, and, if necessary, extend
the head and advance. If difficulty is encountered, perform direct
laryngoscopy and insert tube under direct visualization.
3. Successful intubation occurs when the tube passes through the cords; a
cough may occur and breath sounds will reach maximum intensity if the tube
is correctly positioned. Confirm correct placement by checking for bilateral
breath sounds and expansion of the chest.
4. Confirm proper tube placement with chest x-ray.
Ventilator Management 53
and rate to achieve near-total ventilatory support. Pressure support at
5-15 cm H2O in addition to IMV may be added.
2. ABG should be obtained. Check ABG for adequate ventilation and
oxygenation. If PO2 is adequate and pulse oximetry is >98%, then
titrate FiO2 to a safe level (FIO2<60%) by observing the saturation via
pulse oximetry. Repeat ABG when target FiO2 is reached.
3. Chest x-ray for tube placement, measure cuff pressure q8h
(maintain <20 mm Hg), pulse oximeter, arterial line, and/or monitor
end tidal CO2. Maintain oxygen saturation >90-95%.
Ventilator Management
A. Decreased minute ventilation. Evaluate patient and rule out complica
tions (endotracheal tube malposition, cuff leak, excessive secretions,
bronchospasms, pneumothorax, worsening pulmonary disease, sedative
drugs, pulmonary infection). Readjust ventilator rate to maintain mechani
cally assisted minute ventilation of 10 L/min. If peak airway pressure
(AWP) is >45 cm H2O, decrease tidal volume to 7-8 L/kg (with increase
in rate if necessary), or decrease ventilator flow rate.
B. Arterial saturation >94% and pO2 >100, reduce FIO2 (each 1% decrease
in FIO2 reduces pO2 by 7 mm Hg); once FIO2 is <60%, PEEP may be
reduced by increments of 2 cm H2O until PEEP is 3-5cm H2O. Maintain O2
saturation of >90% (pO2 >60).
C. Arterial saturation <90% and pO2 <60, increase FIO2 up to 60-100%,
then consider increasing PEEP by increments of 3-5 cm H2O (PEEP >10
requires a PA catheter). Add additional PEEP until oxygenation is
adequate with an FIO2 of <60%.
D. Excessively low pH, (pH <7.33 because of respiratory acido
sis/hypercapnia): Increase rate and/or tidal volume. Keep peak airway
pressure <40-50 cm H2O if possible.
E. Excessively high pH (>7.48 because of respiratory alkalosis/hypo
capnia): Reduce rate and/or tidal volume. If the patient is breathing rapidly
above ventilator rate, consider sedation.
F. Patient fighting ventilator: Consider IMV or SIMV mode, or add
sedation with or without paralysis. Paralytic agents should not be used
without concurrent amnesia and/or sedation.
G. Sedation
1. Midazolam (Versed) 0.05 mg/kg IVP x1, then 0.02-0.1 mg/kg/hr IV
infusion. Titrate in increments of 25-50%.
2. Lorazepam (Ativan) 1-2 mg IV ql-2h pm sedation or 0.05 mg/kg IVP
x1, then 0.025-0.2 mg/kg/hr IV infusion. Titrate in increments of 25
50%.
3. Morphine sulfate 2-5 mg IV q1h or 0.03-0.05 mg/kg/h IV infusion (100
mg in 250 mL D5W) titrated.
4. Propofol (Diprivan): 50 mcg/kg bolus over 5 min, then 5-50
mcg/kg/min. Titrate in increments of 5 mcg/kg/min.
H. Paralysis (with simultaneous amnesia)
1. Vecuronium (Norcuron) 0.1 mg/kg IV, then 0.06 mg/kg/h IV infusion;
intermediate acting, maximum neuromuscular blockade within 3-5 min.
Half-life 60 min, OR
Ventilator Weaning
I. Ventilator weaning parameters
A. Patient alert and rested
B. PaO2 >70 mm Hg on FiO2 <50%
C. PaCO2 <50 mm Hg; pH >7.25
Ventilator Weaning 55
E. Vital Capacity >10-15 mL/kg (800-1000 mL)
F. Minute Ventilation (VE) <10 L/min; respirations <24 breaths per min
ventilation (VE).
H. PEEP <5 cm H2O
I. Tidal volume 5-8 mL/kg
56 Pulmonary Embolism
(1) Decrease IMV rate at 30 min intervals by 1-3 breath per min at
each step, starting at rate of 8-10 until a rate for zero is
reached.
(2) If each step is tolerated and ABG is adequate (pH >7.3-7.35),
extubation may be considered.
(3) Alternatively: The patient may be watched on minimal support
(ie, pressure support with CPAP) after IMV rate of zero is
reached. If no deterioration is noted, extubation may be
accomplished.
b. Patients with COPD or prolonged ventilator support (>1 week)
(1) Begin with IMV at frequency of 8 breath/minute, with tidal
volume of 10 mL/kg, with an FiO2 10% greater than previous
setting. Check end-tidal CO2.
(2) ABG should be drawn at 30- and 60-minute intervals to check
for adequate ventilation and oxygenation. If the patient and/or
blood gas deteriorate during weaning trial, then return to
previous stable setting.
(3) Decrease IMV rate in increments of 1-2 breath per hour if the
patient is clinical status and blood gases remain stable. Check
ABG and saturation one-half hour after a new rate is set.
(4) If the patient tolerates an IMV rate of zero, decrease the
pressure to support in increments of 2-5 cm H2O per hour until
a pressure support of 5 cm H2O is reached.
(5) Observe the patient for an additional 24 hours on minimal
support before extubation.
3. Causes of inability to wean patients from ventilators:
Bronchospasm, active pulmonary infection, secretions, small
endotracheal tube, weakness of respiratory muscle, low cardiac output.
Pulmonary Embolism
Approximately 300,000 Americans suffer pulmonary embolism each year.
Among those in whom the condition is diagnosed, 2 percent die within the first
day and 10 percent have recurrent pulmonary embolism.
I. Diagnosis of pulmonary embolism
A. Pulmonary embolism should be suspected in any patient with new
cardiopulmonary symptoms or signs and significant risk factors. If no other
satisfactory explanation can be found in a patient with findings suggestive
of pulmonary embolism, the workup for PE must be pursued to comple
tion.
B. Signs and symptoms of pulmonary embolism. Pleuritic chest pain,
unexplained shortness of breath, tachycardia, hypoxemia, hypotension,
hemoptysis, cough, syncope. The classic triad of dyspnea, chest pain, and
hemoptysis is seen in only 20% of patients. The majority of patients have
only a few subtle symptoms or are asymptomatic.
C. Massive pulmonary emboli may cause the sudden onset of precordial pain,
dyspnea, syncope, or shock. Other findings include distended neck veins,
cyanosis, diaphoresis, pre-cordial heave, a loud pulmonic valve compo
nent of the second heart sound. Right ventricular S3, and a tricuspid
insufficiency.
Ventilator Weaning 57
D. Deep venous thrombosis may manifest as an edematous limb with an
erythrocyanotic appearance, dilated superficial veins, and elevated skin
temperature.
Frequency of Symptoms and Signs in Pulmonary Embolism
Symptoms
Frequency
(%)
Signs
Frequency
(%)
Dyspnea
Pleuritic chest pain
Apprehension
Cough
Hemoptysis
Sweating
Non-pleuritic chest pain
84
74
59
53
30
27
14
Tachypnea (>16/min)
Rales
Accentuated S2
Tachycardia
Fever (>37.8C)
Diaphoresis
S3 or S4 gallop
Thrombophlebitis
92
58
53
44
43
36
34
32
58 Pulmonary Embolism
3. Intermediate V/Q scans are not diagnostic and usually indicate the
need for further diagnostic testing. One-third of patients with inter
mediate scans have a pulmonary embolism and should have a follow
up chest CT or pulmonary angiography.
E. Venous imaging
1. If the V/Q scan is nondiagnostic, a workup for deep venous thrombo
sis (DVT) should be pursued using duplex ultrasound. The identifica
tion of DVT in a patient with signs and symptoms suggesting pulmo
nary embolism proves the diagnosis of pulmonary embolism. A deep
venous thrombosis can be found in 80% of cases of pulmonary
emboli.
2. Inability to demonstrate the existence of a DVT does not significantly
lower the likelihood of pulmonary embolism because clinically
asymptomatic DVT may not be detectable.
3. Patients with a nondiagnostic V/Q scan and no demonstrable site of
DVT should proceed to chest CT or pulmonary angiography.
F. Chest CT may be used in place of pulmonary angiography in patients
with abnormal chest x-ray in whom V/Q scan is nondiagnostic, or in
presence of an intermediate probability of PE on V/Q scan. Chest CT is
associated with fewer complications than pulmonary angiography.
However, chest CT offers a more limited view of this pulmonary field and
does not allow for measurement of pulmonary artery pressure.
G. Angiography. Contrast pulmonary arteriography is the gold standard for
the diagnosis of pulmonary embolism. False-negative results occur in 2
10% of patients. Angiography carries a low risk of complications (minor
5%, major nonfatal 1%, fatal 0.5%).
IV. Management of acute pulmonary embolism in stable patients
A. Oxygen should be initiated for all patients.
B. Antithrombotic therapy
1. Heparin therapy should be started as soon as the diagnosis of
pulmonary embolism is suspected. Full-dose heparin can be given
immediately after major surgery.
2. Unfractionated heparin is administrated as 80 U/kg IVP, then 18
U/kg/h IV infusion. Obtain an aPTT in 6 hours, and adjust dosage
based on the table below to maintain the aPTT between 60-85
seconds. Contraindications to heparin include active internal bleeding
and recent and significant trauma.
Heparin Maintenance Dose Adjustment
aPTTs
Bolus
Dose
Stop infu
sion
Rate Change,
mL/h*
Repeat aPTT
<50
5000 U
0 min
+3 (increase by
150 U/h)
6h
50-59
0 min
+2 (increase by
100 U/h)
6h
60-85
0 min
0 (no change)
next AM
Pulmonary Embolism 59
aPTTs
Bolus
Dose
Stop infu
sion
Rate Change,
mL/h*
Repeat aPTT
86-95
0 min
-1 (decrease by
50 U/h)
next AM
96-120
30 min
-2 (decrease by
100 U/h)
6h
>120
60 min
-3 (decrease by
150 U/h)
6h
*50 U/mL
60 Asthma
isoproterenol, or norepinephrine may be required. Pulmonary artery
pressure monitoring may be helpful.
E. Emergency thoracotomy. Emergency surgical removal of embolized
thrombus is reserved for instances when there is an absolute contraindica
tion to thrombolysis or when the patient's condition has failed to improve
after thrombolysis. Cardiac arrest from pulmonary embolism is an
indication for immediate thoracotomy.
Asthma
Asthma is the most common chronic disease among children. Asthma triggers
include viral infections; environmental pollutants, such as tobacco smoke; as
pirin, nonsteroidal anti-inflammatory drugs, and sustained exercise, particularly
in cold environments.
I. Diagnosis
A. Symptoms of asthma may include episodic complaints of breathing
difficulties, seasonal or nighttime cough, prolonged shortness of breath
after a respiratory infection, or difficulty sustaining exercise.
B. Wheezing does not always represent asthma. Wheezing may persist for
weeks after an acute bronchitis episode. Patients with chronic obstructive
pulmonary disease may have a reversible component superimposed on
their fixed obstruction. Etiologic clues include a personal history of allergic
disease, such as rhinitis or atopic dermatitis, and a family history of allergic
disease.
C. The frequency of daytime and nighttime symptoms, duration of exacerba
tions and asthma triggers should be assessed.
D. Physical examination. Hyperventilation, use of accessory muscles of
respiration, audible wheezing, and a prolonged expiratory phase are
common. Increased nasal secretions or congestion, polyps, and eczema
may be present.
E. Measurement of lung function. An increase in the forced expiratory
volume in one second (FEV1) of 12% after treatment with an inhaled beta2
agonist is sufficient to make the diagnosis of asthma. A 12% change in
peak expiratory flow rate (PEFR) measured on a peak-flow meter is also
diagnostic.
II. Treatment of asthma
A. Beta2 agonists
1. Inhaled short-acting beta2-adrenergic agonists are the most effective
drugs available for treatment of acute bronchospasm and for preven
tion of exercise-induced asthma. Levalbuterol, the R-isomer of racemic
albuterol, offers no significant advantage over racemic albuterol.
2. Salmeterol, a long-acting beta2 agonist, has a relatively slow onset of
action and a prolonged effect. Salmeterol should not be used in the
treatment of acute bronchospasm. Patients taking salmeterol should
use a short-acting beta2 agonist as needed to control acute symptoms.
Twice-daily inhalation of salmeterol has been effective for maintenance
treatment in combination with inhaled corticosteroids.
3. Adverse effects of beta2 agonists. Tachycardia, palpitations, tremor
and paradoxical bronchospasm can occur. High doses can cause
hypokalemia.
Asthma 61
Formulation
Dosage
Albuterol
Proventil
Proventil-HFA
Ventolin
Ventolin Rotacaps
Albuterol
Proventil
multi-dose vials
Ventolin Nebules
Ventolin
nebulized
Levalbuterol - Xopenex
nebulized
Salmeterol
Serevent
Serevent Diskus
2 puffs q12h
Beclomethasone
dipropionate
Beclovent
Vanceril
Vanceril Double-Strength
Budesonide
Pulmicort Turbuhaler
Flunisolide - AeroBid
metered-dose inhaler
(250 :g/puff)
Fluticasone Flovent
metered-dose inhaler
(44, 110 or 220 :g/puff)
dry-powder inhaler (50,
100 or 250 :g/inhalation)
metered-dose inhaler
(100 :g/puff)
1 inhalation q12h
Inhaled Corticosteroids
Flovent Rotadisk
Triamcinolone acetonide
Azmacort
Leukotriene Modifiers
62 Asthma
Drug
Formulation
Dosage
Montelukast - Singulair
tablets
10 mg qhs
Zafirlukast - Accolate
tablets
20 mg bid
Zileuton - Zyflo
tablets
600 mg qid
Cromolyn
Intal
metered-dose inhaler
(800 :g/puff)
Nedocromil
Tilade
metered-dose inhaler
(1.75 mg/puff)
Phosphodiesterase Inhibitor
Theophylline
Slo-Bid Gyrocaps, TheoDur, Unidur
extended-release cap
sules or tablets
100-300 mg bid
B. Inhaled corticosteroids
1. Regular use of an inhaled corticosteroid can suppress inflammation,
decrease bronchial hyperresponsiveness and decrease symptoms.
Inhaled corticosteroids are recommended for treatment of patients
with mild or moderate persistent asthma as well as those with severe
disease.
2. Adverse effects. Inhaled corticosteroids are usually free of toxicity.
Dose-dependent slowing of linear growth may occur within 6-12 weeks
in some children. Decreased bone density, glaucoma and cataract
formation have been reported. Churg-Strauss vasculitis has been
reported rarely. Dysphonia and oral candidiasis can occur. The use of
a spacer device and rinsing the mouth after inhalation decreases the
incidence of candidiasis.
C. Leukotriene modifiers
1. Leukotrienes increase production of mucus and edema of the airway
wall, and may cause bronchoconstriction. Montelukast and zafirlukast
are leukotriene receptor antagonists. Zileuton inhibits synthesis of
leukotrienes.
2. Montelukast (Singulair) is modestly effective for maintenance
treatment of intermittent or persistent asthma. It is taken once daily in
the evening. It is less effective than inhaled corticosteroids, but
addition of montelukast may permit a reduction in corticosteroid
dosage. Montelukast added to oral or inhaled corticosteroids can
improve symptoms.
3. Zafirlukast (Accolate) is modestly effective for maintenance
treatment of mild-to-moderate asthma It is less effective than inhaled
corticosteroids. Taking zafirlukast with food markedly decreases its
bioavailability. Theophylline can decrease its effect. Zafirlukast
increases serum concentrations of oral anticoagulants and may cause
bleeding. Infrequent adverse effects include mild headache, gastroin-
Asthma 63
testinal disturbances and increased serum aminotransferase activity.
Drug-induced lupus and Churg-Strauss vasculitis have been reported.
4. Zileuton (Zyflo) is modestly effective for maintenance treatment, but
it is taken four times a day and patients must be monitored for hepatic
toxicity.
D. Cromolyn (Intal) and nedocromil (Tilade)
1. Cromolyn sodium, an inhibitor of mast cell degranulation, can
decrease airway hyperresponsiveness in some patients with asthma.
The drug has no bronchodilating activity and is useful only for
prophylaxis. Cromolyn has virtually no systemic toxicity.
2. Nedocromil has similar effects as cromolyn. Both cromolyn and
nedocromil are much less effective than inhaled corticosteroids.
E. Theophylline
1. Oral theophylline has a slower onset of action than inhaled beta2
agonists and has limited usefulness for treatment of acute symptoms.
It can, however, reduce the frequency and severity of symptoms,
especially in nocturnal asthma, and can decrease inhaled
corticosteroid requirements.
2. When theophylline is used alone, serum concentrations between 8-12
mcg/mL provide a modest improvement is FEV1. Serum levels of 15
20 mcg/mL are only minimally more effective and are associated with
a higher incidence of cardiovascular adverse events.
F. Oral corticosteroids are the most effective drugs available for acute
exacerbations of asthma unresponsive to bronchodilators.
1. Oral corticosteroids decrease symptoms and may prevent an early
relapse. Chronic use of oral corticosteroids can cause glucose
intolerance, weight gain, increased blood pressure, osteoporosis,
cataracts, immunosuppression and decreased growth in children.
Alternate-day use of corticosteroids can decrease the incidence of
adverse effects, but not of osteoporosis.
2. Prednisone, prednisolone or methylprednisolone (Solu-Medrol),
40-60 mg qd; for children, 1-2 mg/kg/day to a maximum of 60 mg/day.
Therapy is continued for 3-10 days. The oral steroid dosage does not
need to be tapered after short-course burst therapy if the patient is
receiving inhaled steroid therapy.
G.
Choice of drugs
1. Patients with infrequent mild symptoms of asthma may require only
intermittent use, as needed, of a short-acting inhaled beta2-adrenergic
agonist. Overuse of inhaled short-acting beta2 agonists or more than
twice a week indicates that an inhaled corticosteroid should be added
to the treatment regimen.
Pharmacotherapy for Asthma Based on Disease Classification
Classification
Mild intermit
tent
Mild persistent
Quick-relief medications
Classification
Quick-relief medications
Moderate per
sistent
Severe persis
tent
MDI
Aerosol
Albuterol
(Proventil, Ventolin)
Pirbuterol (Maxair)
2 puffs q4-6h
Salmeterol (Serevent)
2 puffs q12h
Pleural Effusion 67
V. Ventilatory assistance
A. Patients with extreme dyspnea, discordant breathing, fatigue, inability to
speak, or deteriorating mental status in the face of adequate therapy may
require ventilatory assistance. Hypoxemia that does not respond to
oxygen therapy or worsening of acid-base status in spite of controlled
oxygen therapy may also require ventilatory assistance.
B. Noninvasive, nasal, or bilevel positive airway pressure (BiPAP) may
improve respiratory rate, tidal volume, and minute ventilation. Patients
successfully treated with noninvasive ventilation have a lower incidence
of pneumonia and sinusitis.
VI. Surgical treatment. Lung volume reduction surgery (LVRS) consists of
surgical removal of an emphysematous bulla. This procedure can ameliorate
symptoms and improve pulmonary function. Lung transplantation is reserved
for those patients deemed unsuitable or too ill for LVRS.
VII. Hypoxemia adversely affects function and increases risk the of death, and
oxygen therapy is the only treatment documented to improve survival in
patients with COPD. Oxygen is usually delivered by nasal cannula at a flow
rate sufficient to maintain an optimal oxygen saturation level.
Pleural Effusion
Pre-thoracentesis chest x-ray: A bilateral decubitus x-ray should be obtained
before the thoracentesis. Thoracentesis is safe when fluid freely layers out
and is greater than 10 mm in depth on the decubitus film.
Labs: CBC, ABG, SMA 12, protein, albumin, amylase, rheumatoid factor, ANA,
ESR. INR/PTT, UA. Chest x-ray PA & LAT repeat after thoracentesis,
bilateral decubitus, ECG.
Pleural fluid analysis:
Tube 1. LDH, protein, amylase, triglyceride, glucose (10 mL).
68 Pleural Effusion
Tube 2. Gram stain, C&S, AFB, fungal C&S, (20-60 mL, heparinized).
heparinized).
Bottle. Cytology.
Differential Diagnosis
Pleural Fluid Param
eters
Transudate
Exudate
LDH (IU)
<200
>200
Pleural LDH/serum
LDH
<0.6
>0.6
<3.0
>3.0
Pleural Protein/serum
Protein
<0.5
>0.5
Pneumothorax 69
Trauma
Blanding U. Jones, MD
Pneumothorax
I. Management of pneumothorax
A. Small primary spontaneous pneumothorax (<10-15%): (not associ
ated with underlying pulmonary diseases). If the patient is not
dyspneic.
1. Observe for 4-8 hours and repeat a chest x-ray.
2. If the pneumothorax does not increase in size and the patient remains
asymptomatic, consider discharge home with instructions to rest and
curtail all strenuous activities. The patient should return if there is an
increase in dyspnea or recurrence of chest pain.
B. Secondary spontaneous pneumothorax (associated with underlying
pulmonary pathology, emphysema) or primary spontaneous
pneumothorax >15%, or if patient is symptomatic.
1. Give high-flow oxygen by nasal cannula. A needle thoracotomy should
be placed at the anterior, second intercostal space in the midclavicular
line.
2. Anesthetize and prep the area, then insert a 16-gauge needle with an
internal catheter and a 60 mL syringe, attached via a 3-way stopcock.
Aspirate until no more air is aspirated. If no additional air can be
aspirated, and the volume of aspirated air is <4 liters, occlude the
catheter and observe for 4 hours.
3. If symptoms abate and chest-x-ray does not show recurrence of the
pneumothorax, the catheter can be removed, and the patient can be
discharged home with instructions.
4. If the aspirated air is >4 liters and additional air is aspirated without
resistance, this represents an active bronchopleural fistula with
continued air leak. Admission is required for insertion of a chest tube.
C. Traumatic pneumothorax associated with a penetrating injury,
hemothorax, mechanical ventilation, tension pneumothorax, or if
pneumothorax does not resolve after needle aspiration: Give high
flow oxygen and insert a chest tube. Do not delay the management of a
tension pneumothorax until radiographic confirmation; insert needle
thoracotomy or chest tube immediately.
D. Iatrogenic pneumothorax
1. Iatrogenic pneumothoraces include lung puncture caused by
thoracentesis or central line placement.
2. Administer oxygen by nasal cannula.
3. If the pneumothorax is less than 10% and the patient is asymp
tomatic, observe and repeat chest x-ray in 4 hours. If unchanged,
manage expectantly with close follow-up, and repeat chest x-ray in 24
hours.
4. If the pneumothorax is more than 10% and/or the patient is
symptomatic, perform a tube thoracostomy under negative pressure.
70 Tension Pneumothorax
II. Technique of chest tube insertion
A. Place patient in supine position, with involved side elevated 20 degrees.
Abduct the arm to 90 degrees. The usual site is the fourth or fifth
intercostal space, between the mid-axillary and anterior axillary line
(drainage of air or free fluid). The point at which the anterior axillary fold
meets the chest wall is a useful guide. Alternatively, the second or third
intercostal space, in the midclavicular line, may be used for pneumothorax
drainage alone (air only).
B. Cleanse the skin with Betadine iodine solution, and drape the field.
Determine the intrathoracic tube distance (lateral chest wall to the apices),
and mark the length of tube with a clamp.
C. Infiltrate 1% lidocaine into the skin, subcutaneous tissues, intercostal
muscles, periosteum, and pleura using a 25-gauge needle. Use a scalpel
to make a transverse skin incision, 2 centimeters wide, located over the
rib, just inferior to the interspace where the tube will penetrate the chest
wall.
D. Use a Kelly clamp to bluntly dissect a subcutaneous tunnel from the skin
incision, extending just over the superior margin of the lower rib. Avoid the
nerve, artery and vein located at the upper margin of the intercostal
space.
E. Penetrate the pleura with the clamp, and open the pleura 1 centimeter.
With a gloved finger, explore the subcutaneous tunnel, and palpate the
lung medially. Exclude possible abdominal penetration, and ensure
correct location within pleural space; use finger to remove any local
pleural adhesions.
F. Use the Kelly clamp to grasp the tip of the thoracostomy tube (36 F,
internal diameter 12 mm), and direct it into the pleural space in a
posterior, superior direction for pneumothorax evacuation. Direct the tube
inferiorly for pleural fluid removal. Guide the tube into the pleural space
until the last hole is inside the pleural space and not inside the subcutane
ous tissue.
G. Attach the tube to a underwater seal apparatus containing sterile normal
saline, and adjust to 20 cm H2O of negative pressure, or attach to suction
if leak is severe. Suture the tube to the skin of the chest wall using O silk.
Apply Vaseline gauze, 4 x 4 gauze sponges, and elastic tape. Obtain a
chest x-ray to verify correct placement and evaluate reexpansion of the
lung.
Tension Pneumothorax
I. Clinical evaluation
A. Clinical signs: Severe hemodynamic and/or respiratory compromise;
contralaterally deviated trachea; decreased or absent breath sounds and
hyperresonance to percussion on the affected side; jugular venous
distention, asymmetrical chest wall motion with respiration.
B. Radiologic signs: Flattening or inversion of the ipsilateral
hemidiaphragm; contralateral shifting of the mediastinum; flattening of the
cardio-mediastinal contour and spreading of the ribs on the ipsilateral
side.
Cardiac Tamponade 71
II. Acute management
A. A temporary large-bore IV catheter may be inserted into the ipsilateral
pleural space, at the level of the second intercostal space at the
midclavicular line until the chest tube is placed.
B. A chest tube should be placed emergently.
C. Draw blood for CBC, INR, PTT, type and cross-matching, chem 7,
toxicology screen.
D. Send pleural fluid for hematocrit, amylase and pH (to rule out esophageal
rupture).
E. Indications for cardiothoracic exploration: Severe or persistent
hemodynamic instability despite aggressive fluid resuscitation, persistent
active blood loss from chest tube, more than 200 cc/hr for 3 consecutive
hours, or $1 L of acute blood loss after chest tube placement.
Cardiac Tamponade
I. General considerations
A. Cardiac tamponade occurs most commonly secondary to penetrating
injuries.
B. Beck's Triad: Venous pressure elevation, drop in the arterial pressure,
muffled heart sounds. Other signs include enlarged cardiac silhouette on
chest x-ray; signs and symptoms of hypovolemic shock; pulseless
electrical activity, decreased voltage on ECG.
C. Kussmaul's sign is characterized by a rise in venous pressure with
inspiration. Pulsus paradoxus or elevated venous pressure may be
absent when associated with hypovolemia.
II. Management
A. Pericardiocentesis is indicated if the patient is unresponsive to resuscita
tion measures for hypovolemic shock, or if there is a high likelihood of
injury to the myocardium or one of the great vessels.
B. All patients who have a positive pericardiocentesis (recovery of non
clotting blood) because of trauma, require an open thoracotomy with
inspection of the myocardium and the great vessels.
C. Rule out other causes of cardiac tamponade such as pericarditis,
penetration of central line through the vena cava, atrium, or ventricle, or
infection.
D. Consider other causes of hemodynamic instability that may mimic cardiac
tamponade (tension pneumothorax, massive pulmonary embolism, shock
secondary to massive hemothorax).
Pericardiocentesis
I. General considerations
A. If acute cardiac tamponade with hemodynamic instability is suspected,
emergency pericardiocentesis should be performed; infusion of Ringer's
lactate, crystalloid, colloid and/or blood may provide temporizing mea
sures.
72 Pericardiocentesis
II. Management
A. Protect airway and administer oxygen. If patient can be stabilized,
pericardiocentesis should be performed in the operating room or catheter
lab. The para-xiphoid approach is used for pericardiocentesis.
B. Place patient in supine position with chest elevated at 30-45 degrees,
then cleanse and drape peri-xiphoid area. Infiltrate lidocaine 1% with
epinephrine (if time permits) into skin and deep tissues.
C. Attach a long, large bore (12-18 cm, 16-18 gauge), short bevel cardiac
needle to a 50 cc syringe with a 3-way stop cock. Use an alligator clip to
attach a V-lead of the ECG to the metal of the needle.
D. Advance the needle just below costal margin, immediately to the left and
inferior to the xiphoid process. Apply suction to the syringe while advanc
ing the needle slowly at a 45 -degree horizontal angle towards the mid
point of the left clavicle.
E. As the needle penetrates the pericardium, resistance will be felt, and a
popping sensation will be noted.
F. Monitor the ECG for ST segment elevation (indicating ventricular heart
muscle contact); or PR segment elevation (indicating atrial epicardial
contact). After the needle comes in contact with the epicardium, withdraw
the needle slightly. Ectopic ventricular beats are associated with cardiac
penetration.
G. Aspirate as much blood as possible. Blood from the pericardial space
usually will not clot. Blood, inadvertently, drawn from inside the ventricles
or atrium usually will clot. If fluid is not obtained, redirect the needle more
towards the head. Stabilize the needle by attaching a hemostat or Kelly
clamp.
H. Consider emergency thoracotomy to determine the cause of
hemopericardium (especially if active bleeding). If the patient does not
improve, consider other problems that may resemble tamponade, such as
tension pneumothorax, pulmonary embolism, or shock secondary to
massive hemothorax.
References
Committee on Trauma, American College of Surgeons: Early Care of the Injured Patient.
Philadelphia, WB Sanders Co., 1982, pp 142-148.
Light RW. Management of Spontaneous Pneumothorax. Am. Rev. Res. Dis. 1993; 148, 1:
245-248.
Light RW. Pneumothorax. In: Light RW, ed. Pleural Diseases. Philadelphia; Lea &
Farbiger, 1990; 237-62.
Transfusion Reactions 73
Hematologic Disorders
Thomas Vovan, MD
Transfusion Reactions
I.
Thrombolytic-associated Bleeding 75
then be followed to guide therapy. The heparin dose may be increased
by 2.5 U/kg/hr until the desired effect is achieved.
Thrombolytic-associated Bleeding
I. Clinical presentation: Post-fibrinolysis hemorrhage may present as a sudden
neurologic deficit (intracranial bleeding), massive GI bleeding, progressive
back pain accompanied by hypotension (retroperitoneal bleeding), or a
gradual decline in hemoglobin without overt evidence of bleeding.
II. Laboratory evaluation
A. Low fibrinogen (<100 mg/dL) and elevated fibrin degradation products
confirm the presence of a lytic state. Elevated thrombin time and PTT may
suggest a persistent lytic state; however, both are prolonged in the
presence of heparin. Prolonged reptilase time identifies the persistent lytic
state in the presence of heparin.
B. Depleted fibrinogen in the fibrinolytic state will be reflected by an elevated
PTT, thrombin time, or reptilase time. The post-transfusion fibrinogen level
is a useful indicator of response to replacement therapy.
C. The bleeding time may be a helpful guide to platelet replacement therapy
if the patient has persistent bleeding despite factor replacement with
cryoprecipitate and fresh frozen plasma.
III.
Management
A. Discontinue thrombolytics, aspirin, and heparin immediately, and consider
protamine reversal of heparin and cryoprecipitate to replenish fibrinogen.
B. Place two large-bore IV catheters for volume replacement. If possible,
apply local pressure to bleeding sites. Blood specimens should be sent for
INR/PTT, fibrinogen, and thrombin time. Reptilase time should be checked
if the patient is also receiving heparin. Patient's blood should be typed and
crossed because urgent transfusion may be needed.
C. Transfusion
1. Cryoprecipitate (10 units over 10 minutes) should be transfused to
correct the lytic state. Transfusions may be repeated until the fibrinogen
level is above 100 mg/dL or hemostasis is achieved. Cryoprecipitate is
rich in fibrinogen and factor VIII.
2. Fresh frozen plasma transfusion is also important for replacement of
factor VIII and V. If bleeding persists after cryoprecipitate and FFP
replacement, check a bleeding time and consider platelet transfusion
if bleeding time is greater than 9 minutes. If bleeding time is less than
9 minutes, then antifibrinolytic drugs may be warranted.
D. Antifibrinolytic agents
1. Aminocaproic acid (EACA) inhibits the conversion of plasminogen to
plasmin. It is used when replacement of blood products are not
sufficient to attain hemostasis.
2. Loading dose: 5 g or 0.1 g/kg IV infused in 250 cc NS over 30-60 min,
followed by continuous infusion at 0.5-2.0 g/h until bleeding is con
trolled. Use with caution in upper urinary tract bleeding because of the
potential for obstruction.
References
Carr JM, McKinney M, McDonagh J: Diagnosis of Disseminated Intravascular Coagulation,
Role of D-Dimer. Am J Clin Pathol 1989;91:280-287.
76 Thrombolytic-associated Bleeding
Feinstein DI: Treatment of Disseminated Intravascular Coagulation. Seminars in Thrombosis
and Hemostasis. 1988;14:351-362.
Sane DC, Califf RM, Topol EJ, Stump DC, Mark DB, Greenberg CS: Bleeding during
Thrombolytic Therapy for Acute Myocardial Infarction: Mechanisms and Management.
Ann of Int Med. 1989;111:1010-1022.
Bacterial Meningitis 77
Infectious Diseases
Guy Foster, MD
Farhad Mazdisnian, MD
Michael Krutzik, MD
Georgina Heal, MD
Bacterial Meningitis
The age group at greatest risk for acute bacterial meningitis (ABM) includes
children between 1 and 24 months of age. Adults older than 60 years old account
for 50% of all deaths related to meningitis.
I. Clinical presentation
A. Eighty-five percent of patients with bacterial meningitis present with fever,
headache, meningismus or nuchal rigidity, and altered mental status.
Other common signs and symptoms include photophobia, vomiting, back
pain, myalgias, diaphoresis, and malaise. Generalized seizures can occur
in up to 40% of patients with ABM.
B. Kernig's sign (resistance to extension of the leg while the hip is flexed) and
Brudzinski's sign (involuntary flexion of the hip and knee when the patient's
neck is abruptly flexed while laying supine) are observed in up to 50% of
patients.
C. About 50% of patients with N. meningitidis may present with an
erythematous macular rash, which progresses to petechiae and purpura.
II. Patient evaluation
A. Computerized tomography (CT). Patients who require CT prior to LP
include those with focal neurologic findings, papilledema, focal seizures,
or abnormalities on exam that suggest increased intracranial pressure. If
bacterial meningitis is a strong consideration, and the decision is made to
perform a CT prior to LP, two sets of blood cultures should be obtained
and antibiotics should be administered before sending the patient for
neuroimaging. Urine cultures may be helpful in the very young and very
old.
B. Blood cultures followed by antibiotic administration within 30 minutes of
presentation is mandatory in all patients suspected of having bacterial
meningitis.
C. Interpretation of lumbar puncture. Examination of the CSF is mandatory
for evaluation of meningitis.
D. CSF, Grams stain, and culture are positive in 70-85% of patients with
ABM.
78 Bacterial Meningitis
WBC
count
(WBC/
:L)
% PMN
Normal
Bacterial
Viral
Fungal
TB
Para
menin
geal
Focus
or Ab
scess
0-5
>1000
100
1000
100-500
100
500
10-1000
0-15
90
<50
<50
<50
<50
>50
>50
>80
%
lymph
Glucose
(mg/
dL)
45-65
<40
45
65
30-45
30
45
45-65
CSF:
blood
glucose
ratio
0.6
<0.4
0.6
<0.4
<0.4
0.6
Protein
(mg/dL)
20-45
>150
50
100
100-500
100
500
>50
Open
ing
press
ure
(cm
H20)
6-20
>180 mm
H20
NL or
+
>180
mm H20
>180
mm
H20
N/A
E. If the CSF parameters are nondiagnostic, or the patient has been treated
with prior oral antibiotics, and, therefore, the Gram's stain and/or culture
are likely to be negative, then latex agglutination (LA) may be helpful. The
test has a variable sensitivity rate, ranging between 50-100%, and high
specificity. Latex agglutination tests are available for H. influenza,
Streptococcus pneumoniae, N. meningitidis, Escherichia coli K1, and S.
agalactiae (Group B strep). CSF Cryptococcal antigen and India ink stain
should be considered in patients who have HIV disease or HIV risk
factors.
Bacterial Meningitis 79
III. Treatment of acute bacterial meningitis
Antibiotic Choice Based on Age and Comorbid Medical Illness
Age
Organism
Antibiotic
Neonate
1-3 months
S. pneumoniae, N.
meningitidis, H.
influenzae, S. agalactiae,
Listeria, E. coli
Ceftriaxone or cefotaxime
and vancomycin
3 months to 18 years
N. meningitidis, S.
pneumoniae, H.
influenzae
Ceftriaxone or cefotaxime
and vancomycin
18-50 years
S. pneumoniae, N.
meningitidis
Ceftriaxone or cefotaxime
and vancomycin
N. meningitidis, S.
pneumoniae
Gram-negative bacilli, Lis
teria, Group B strep
Neurosurgery/head
injury
S. aureus, S. epidermidis
Diphtheroids, Gram-nega
tive bacilli
Vancomycin and
Ceftazidime
Immunosuppression
Listeria, Gram-negative
bacilli, S. pneumoniae, N.
meningitidis
CSF shunt
S. aureus, Gram-negative
bacilli
Vancomycin and
Ceftazidime
Organism
Antibiotic
S. pneumoniae
S. aureus, S. agalactiae
(Group B)
Vancomycin and
ceftriaxone or cefotaxime
N. meningitidis
Penicillin G or
chloramphenicol
H. influenzae
Third-generation
cephalosporin
80 Bacterial Meningitis
Stain Results
Organism
Antibiotic
Listeria monocytogenes
Ampicillin, Penicillin G +
IV Gentamicin
intrathecal gentamicin
E. coli, Klebsiella
Serratia, Pseudomonas
Ceftazidime +/
aminoglycoside
Dosage
Ampicillin
2 g IV q4h
Cefotaxime
2 g IV q4-6h
Ceftazidime
2 g IV q8h
Ceftriaxone
2 g IV q12h
Chloramphenicol
0.5-1.0 gm IV q6h
Gentamicin
Nafcillin/Oxacillin
2 g IV q4h
Penicillin G
Rifampin
600 mg PO q24h
Trimethoprim-sulfamethoxazole
15 mg/kg IV q6h
Vancomycin
1.0-1.5 g IV q12h
Pneumonia 81
C. Corticosteroids. Audiologic and neurological sequelae in infants older
than two months of age are markedly reduced by early administration of
dexamethasone in patients with H. influenzae meningitis. Dexametha
sone should be given at a dose of 0.15 mg/kg q6h IV for 2-4 days to
children with suspected H. influenzae or pneumococcal meningitis. The
dose should be given just prior to or with the initiation of antibiotics.
Pneumonia
Community-acquired pneumonia is the leading infectious cause of death and is
the sixth-leading cause of death overall.
I.
Clinical diagnosis
A. Symptoms of pneumonia may include fever, chills, malaise and cough.
Patients also may have pleurisy, dyspnea, or hemoptysis. Eighty percent
of patients are febrile.
B. Physical exam findings may include tachypnea, tachycardia, rales,
rhonchi, bronchial breath sounds, and dullness to percussion over the
involved area of lung.
C. Chest radiograph usually shows infiltrates. The chest radiograph may
reveal multilobar infiltrates, volume loss, or pleural effusion. The chest
radiograph may be negative very early in the illness because of dehy
dration or severe neutropenia.
D. Additional testing may include a complete blood count, pulse oximetry
or arterial blood gas analysis.
II. Laboratory evaluation
A. Sputum for Gram stain and culture should be obtained in hospitalized
patients. In a patient who has had no prior antibiotic therapy, a high
quality specimen (>25 white blood cells and <5 epithelial cells/hpf) may
help to direct initial therapy.
B. Blood cultures are positive in 11% of cases, and cultures may identify
a specific etiologic agent.
C. Serologic testing for HIV is recommended in hospitalized patients
between the ages of 15 and 54 years. Urine antigen testing for
legionella is indicated in endemic areas for patients with serious
pneumonia.
III. Indications for hospitalization
A. Age >65years
B. Unstable vital signs (heart rate >140 beats per minute, systolic blood
pressure <90 mm Hg, respiratory rate >30 beats per minute)
C. Altered mental status
82 Pneumonia
Less Common
Streptococcus pneumoniae
Haemophilus influenzae
Moraxella catarrhalis
Mycoplasma pneumoniae
Chlamydia pneumoniae
Legionella species
Viruses
Anaerobes (especially with aspiration)
Staphylococcus aureus
Gram-negative bacilli
Pneumocystis carinii
Mycobacterium tuberculosis
Primary Treatment
Alternative(s)
Macrolide antibiotics
(azithromycin,
clarithromycin,
dirithromycin, or
erythromycin)
Levofloxacin or doxycycline
Levofloxacin or
cefuroxime or
Trimethoprim-sulfa
methoxazole
Add vancomycin in
severe, life-threaten
ing pneumonias
Clindamycin IV
Cefotetan,
ampicillin/sulbactam
Pneumonia 83
2. A second-generation cephalosporin (eg, cefuroxime [Ceftin]) is
recommended for initial empirical treatment. Trimethoprim
sulfamethoxazole is an inexpensive alternative where pneumococcal
resistance to not prevalent.
3. When legionella infection is suspected, initial therapy should include
treatment with a macrolide antibiotic in addition to a beta-lactam/beta
lactamase inhibitor (amoxicillin clavulanate).
C. Moderately ill, hospitalized patients
1. In addition to S pneumoniae and H influenzae, more virulent patho
gens, such as S aureus, Legionella species, aerobic gram-negative
bacilli (including P aeruginosa, and anaerobes), should be considered
in patients requiring hospitalization.
2. Hospitalized patients should receive an intravenous cephalosporin
active against S pneumoniae and anaerobes (eg, cefuroxime,
ceftriaxone [Rocephin], cefotaxime [Claforan]), or a beta-lactam/beta
lactamase inhibitor.
3. Nosocomial pneumonia should be suspected in patients with recent
hospitalization or nursing home status. Nosocomial pneumonia is most
commonly caused by Pseudomonas or Staph aureus. Empiric therapy
should consist of vancomycin and double pseudomonal coverage with
a beta-lactam (cefepime, Zosyn, imipenem, ticarcillin, ceftazidime,
cefoperazone) and an aminoglycoside (amikacin, gentamicin,
tobramycin) or a quinolone (ciprofloxacin).
4. When legionella is suspected (in endemic areas, cardiopulmonary
disease, immune compromise), a macrolide should be added to the
regimen. If legionella pneumonia is confirmed, rifampin (Rifadin)
should be added to the macrolide.
Common Antimicrobial Agents for Community-Acquired Pneumonia
in Adults
Type
Agent
Dosage
Macrolides
Erythromycin
Clarithromycin (Biaxin)
Azithromycin (Zithromax)
500 mg PO qid
500 mg PO bid
500 mg PO on day 1, then
250 mg qd x 4 days
Beta-lactam/beta
lactamase inhibitor
Amoxicillin-clavulanate
(Augmentin)
Quinolones
Ciprofloxacin (Cipro)
Levofloxacin (Levaquin)
Ofloxacin (Floxin)
500 mg PO bid
500 mg PO qd
400 mg PO bid
Tetracycline
Doxycycline
100 m g PO bid
Sulfonamide
Trimethoprim
sulfamethoxazole
Oral therapy
84 Pneumonia
Type
Agent
Dosage
Cefuroxime (Kefurox,
Zinacef)
Ceftizoxime (Cefizox)
Ceftazidime (Fortaz)
Cefoperazone (Cefobid)
0.75-1.5 g IV q8h
Ampicillin-sulbactam
(Unasyn)
Piperacillin/tazobactam
(Zosyn)
Ticarcillin-clavulanate
(Timentin)
1.5 g IV q6h
Quinolones
Ciprofloxacin (Cipro)
Levofloxacin (Levaquin)
Ofloxacin (Floxin)
400 mg IV q12h
500 mg IV q24h
400 mg IV q12h
Aminoglycosides
Gentamicin
Amikacin
Vancomycin
Vancomycin
1 gm IV q12h
Intravenous Therapy
Cephalosporins
Second-generation
Third-generation
(anti-Pseudomonas
aeruginosa)
Beta-lactam/beta
lactamase inhibitors
1-2 g IV q8h
1-2 g IV q8h
1-2 g IV q8h
3.375 g IV q6h
3.1 g IV q6h
86 Pneumonia
C. Open-lung biopsy should be reserved for patients with progressive
pulmonary disease in whom the less invasive procedures are
nondiagnostic.
IV. Diagnostic algorithm
A. If the chest radiograph of a symptomatic patient appears normal, a DLCO
should be performed. Patients with significant symptoms, a normal
appearing chest radiograph, and a normal DLCO should undergo high
resolution CT. Patients with abnormal findings at any of these steps
should proceed to sputum induction or bronchoscopy. Sputum specimens
collected by induction that reveal P. carinii should also be stained for
acid-fast organisms and fungi, and the specimen should be cultured for
mycobacteria and fungi.
B. Patients whose sputum examinations do not show P. carinii or another
pathogen should undergo bronchoscopy.
C. Lavage fluid is stained for P. carinii, acid-fast organisms, and fungi. Also,
lavage fluid is cultured for mycobacteria and fungi and inoculated onto
cell culture for viral isolation. Touch imprints are made from tissue
specimens and stained for P. carinii. Fluid is cultured for mycobacteria
and fungi, and stained for P. carinii, acid-fast organisms, and fungi. If all
procedures are nondiagnostic and the lung disease is progressive, open
lung biopsy may be considered.
V. Therapy and prophylaxis
A. Trimethoprim-sulfamethoxazole DS (Bactrim DS, Septra DS) is the
recommended initial therapy for PCP. Dosage is 15-20 mg/kg/day of TMP
IV divided q6h for 14-21 days. Adverse effects include rash (33%),
elevation of liver enzymes (44%), nausea and vomiting (50%), anemia
(40%), creatinine elevation (33%), and hyponatremia (94%).
B. Pentamidine is an alternative in patients who have adverse reactions or
fail to respond to TMP-SMX. The dosage is 4 mg/kg/day IV for 14-21
days. Adverse effects include anemia (33%), creatinine elevation (60%),
LFT elevation (63%), and hyponatremia (56%). Pancreatitis, hypo
glycemia, and hyperglycemia are common side effects.
C. Corticosteroids. Adjunctive corticosteroid treatment is beneficial with
anti-PCP therapy in patients with a partial pressure of oxygen (PaO2) less
than 70 mm Hg, (A-a)DO2 greater than 35 mm Hg, or oxygen saturation
less than 90% on room air. Contraindications include suspected
tuberculosis or disseminated fungal infection. Treatment with methyl
prednisolone (SoluMedrol) should begin at the same time as anti-PCP
therapy. The dosage is 30 mg IV q12h x 5 days, then 30 mg IV qd x 5
days, then 15 mg qd x 11 days OR prednisone, 40 mg twice daily for 5
days, then 40 mg daily for 5 days, and then 20 mg daily until day 21 of
therapy.
VI. Prophylaxis
A. HIV-infected patients who have CD4 counts less than 200 cells/mcL
should receive prophylaxis against PCP. If CD4 count increases to
greater than 200 cells/mcL after receiving antiretroviral therapy, PCP
prophylaxis can be safely discontinued.
B. Trimethoprim-sulfamethoxazole (once daily to three times weekly) is
the preferred regimen for PCP prophylaxis.
Antiretroviral therapy
B. Nucleoside analogs
2. Didanosine (Videx) 200 mg PO bid [chewable tabs: 25, 50, 100, 150
C. Protease inhibitors
D. Non-nucleoside analogs
OR
OR
times/d.
improved.
VII.
Cytomegalovirus infections
A. Ganciclovir (Cytovene) 5 mg/kg IV (dilute in 100 mL D5W over 60 min)
q12h x 14-21 days (concurrent use with zidovudine increases hematolog
ical toxicity).
B. Suppressive treatment for CMV: Ganciclovir (Cytovene) 5 mg/kg IV qd,
or 6 mg/kg IV 5 times/wk, or 1000 mg orally tid with food.
VIII. Toxoplasmosis
A. Pyrimethamine 200 mg PO loading dose, then 50-75 mg qd plus
leucovorin calcium (folinic acid) 10-20 mg PO qd for 6-8 weeks for acute
therapy AND
B. Sulfadiazine (1.0-1.5 gm PO q6h) or clindamycin 450 mg PO qid/600-900
mg IV q6h.
C. Suppressive treatment for toxoplasmosis
1. Pyrimethamine 25-50 mg PO qd with or without sulfadiazine 0.5-1.0
gm PO q6h; and folinic acid 5-10 mg PO qd OR
2. Pyrimethamine 50 mg PO qd; and clindamycin 300 mg PO q6h; and
folinic acid 5-10 mg PO qd.
IX. Cryptococcus neoformans meningitis
A. Amphotericin B at 0.7 mg/kg/d IV for 14 days or until clinically stable,
followed by fluconazole (Diflucan) 400 mg qd to complete 10 weeks of
therapy, followed by suppressive therapy with fluconazole (Diflucan) 200
mg PO qd indefinitely.
B. Amphotericin B lipid complex (Abelcet) may be used in place of non
liposomal amphotericin B if the patient is intolerant to non-liposomal
amphotericin B. The dosage is 5 mg/kg IV q24h.
X. Active tuberculosis
A. Isoniazid (INH) 300 mg PO qd; and rifabutin 300 mg PO qd; and
pyrazinamide 15-25 mg/kg PO qd (500 mg PO bid-tid); and ethambutol
15-25 mg/kg PO qd (400 mg PO bid-tid).
B. All four drugs are continued for 2 months; isoniazid and rifabutin
(depending on susceptibility testing) are continued for a period of at least
9 months and at least 6 months after the last negative cultures.
C. Pyridoxine (vitamin B6) 50 mg PO qd, concurrent with INH.
XI. Disseminated mycobacterium avium complex (MAC)
A. Azithromycin (Zithromax) 500-1000 mg PO qd or clarithromycin (Biaxin)
500 mg PO bid; AND
B. Ethambutol 15-25 mg/kg PO qd (400 mg bid-tid) AND
C. Rifabutin 300 mg/d (two 150 mg tablets qd).
D. Prophylaxis for MAC
1. Clarithromycin (Biaxin) 500 mg PO bid OR
2. Rifabutin (Mycobutin) 300 mg PO qd or 150 mg PO bid.
XII.
Disseminated coccidioidomycosis
A. Amphotericin B (Fungizone) 0.8 mg/kg IV qd OR
B. Amphotericin B lipid complex (Abelcet) 5 mg/kg IV q24h OR
C. Fluconazole (Diflucan) 400-800 mg PO or IV qd.
XIII. Disseminated histoplasmosis
A. Amphotericin B (Fungizone) 0.5-0.8 mg/kg IV qd, until total dose 15
mg/kg OR
B. Amphotericin B lipid complex (Abelcet) 5 mg/kg IV q24h OR
C. Itraconazole (Sporanox) 200 mg PO bid.
Sepsis 89
D. Suppressive treatment for histoplasmosis: Itraconazole (Sporanox)
200 mg PO bid.
Sepsis
Sepsis is the most common cause of death in medical and surgical ICUs. Mortal
ity ranges from 20-60%. The systemic inflammatory response syndrome (SIRS)
is an inflammatory response that is a manifestation of both sepsis and the
inflammatory response that results from trauma or burns. The term sepsis is
reserved for patients who have SIRS attributable to infection.
I.
Pathophysiology
A. Although gram-negative bacteremia is commonly found in patients with
sepsis, gram-positive infection may affect 30-40% of patients. Fungal,
viral and parasitic infections are usually encountered in
immunocompromised patients.
Defining sepsis and related disorders
Term
Definition
Systemic inflamma
tory response syn
drome (SIRS)
Sepsis
Septic shock
90 Sepsis
II. Clinical evaluation
A. Although fever is the most common sign of sepsis, normal body tempera
tures and hypothermia are common in the elderly. Tachypnea and/or
hyperventilation with respiratory alkalosis may occur before the onset of
fever or leukocytosis. Other common clinical signs of systemic inflamma
tion or impaired organ perfusion include altered mentation, oliguria, and
tachycardia.
B. In the early stages of sepsis, tachycardia is associated with increased
cardiac output; peripheral vasodilation; and a warm, well-perfused
appearance. As shock progresses, vascular resistance continues to fall,
hypotension ensues and myocardial depression results in decreased
cardiac output. During the later stages of septic shock, vasoconstriction
and cold extremities develop.
C. Laboratory findings. In the early stages of sepsis, arterial blood gas
measurements usually reveal respiratory alkalosis. As shock ensues,
metabolic acidosis becomes apparent. Hypoxemia is common.
Manifestations of Sepsis
Clinical features
Temperature instability
Tachypnea
Hyperventilation
Altered mental status
Oliguria
Tachycardia
Peripheral vasodilation
Laboratory findings
Respiratory alkaloses
Hypoxemia
Increased serum lactate levels
Leukocytosis and increased neutrophil
concentration
Eosinopenia
Thrombocytopenia
Anemia
Proteinuria
Mildly elevated serum bilirubin levels
D. Hemodynamics
1. The hallmark of early septic shock is a dramatic drop in systemic
vascular resistance, resulting in a decrease in blood pressure.
2. Cardiac output rises in response to the fall in systemic blood pressure.
This is referred to as the hyperdynamic state in sepsis. Shock results
if the increase in cardiac output is insufficient to maintain blood
pressure. Diminished cardiac output may occur as systemic blood
pressure falls.
III. Treatment of sepsis
A. Resuscitation. During the initial resuscitation of a hypotensive patient
with sepsis, large volumes of IV fluid should be given. Initial resuscitation
may require 4-6 L of crystalloid. Fluid infusion volumes should be titrated
to obtain a pulmonary capillary wedge pressure of 10-20 mm Hg. Other
indices of organ perfusion include oxygen delivery, serum lactate levels,
arterial blood pressure, and urinary output.
B. Vasopressor and inotropic therapy is necessary if hypotension persists
despite aggressive fluid resuscitation.
1. Dopamine is a first-line agent for sepsis-associated hypotension.
Begin with 5 :g/kg/min and titrate the dosage to the desired blood
pressure response, usually a systolic blood pressure of greater than
90 mm Hg.
Sepsis 91
2. Norepinephrine or phenylephrine infusions may be used if
hypotension persists despite high dosages of dopamine (20
:g/kg/min), or if dopamine causes excessive tachycardia. These
agents have alpha-adrenergic effects, causing peripheral vaso
constriction and increased the mean arterial pressure.
3. Dobutamine can be added to increase cardiac output through its
beta-adrenergic inotropic effects.
4. Epinephrine has both alpha- and beta-adrenergic properties.
Epinephrine may be added if hypotension persists despite maximum
doses of dopamine and norepinephrine.
C. Activated protein C is a vitamin K-dependent plasma protein which limits
coagulation and augments fibrinolysis. In severe sepsis, activated protein
C (24 mcg/kg/hr for 96 hours) has been shown to decrease mortality from
30.8 to 24.7%. It should not be used in patients with thrombocytopenia,
coagulopathy, recent surgery or recent hemorrhage because it increases
the risk of bleeding.
Vasoactive and Inotropic Drugs
Agent
Dosage
Dopamine
Dobutamine
Norepinephrine
Phenylephrine
Epinephrine
92 Sepsis
Dosage
Cefotaxime (Claforan)
2 gm q4-6h
Ceftizoxime (Cefizox)
2 gm IV q8h
Cefoxitin (Mefoxin)
2 gm q6h
Cefotetan (Cefotan)
2 gm IV q12h
Ceftazidime (Fortaz)
2 g IV q8h
Ticarcillin/clavulanate (Timentin)
Ampicillin/sulbactam (Unasyn)
3.0 gm IV q6h
Piperacillin/tazobactam (Zosyn)
3.375-4.5 gm IV q6h
3 gm IV q4-6h
Meropenem (Merrem)
1 gm IV q8h
Imipenem/cilastatin (Primaxin)
1.0 gm IV q6h
Gentamicin or tobramycin
Amikacin (Amikin)
Vancomycin
1 gm IV q12h
Metronidazole (Flagyl)
500 mg IV q6-8h
Linezolid (Zyvox)
Quinupristin/dalfopristin (Synercid)
Peritonitis 93
not enterococcus faecalis. Most strains of VRE are enterococcus
faecium.
Peritonitis
I. Acute Peritonitis
A. Acute peritonitis is inflammation of the peritoneum or peritoneal fluid from
bacteria or intestinal contents in the peritoneal cavity. Secondary
peritonitis results from perforation of a viscus caused by acute appendici
tis or diverticulitis, perforation of an ulcer, or trauma. Primary peritonitis
refers to peritonitis arising without a recognizable preceding cause.
Tertiary peritonitis consists of persistent intra-abdominal sepsis without
a discrete focus of infection, usually occurring after surgical treatment of
peritonitis.
B. Clinical features
1. Acute peritonitis presents with abdominal pain, abdominal tenderness,
and the absence of bowel sounds. Severe, sudden-onset abdominal
pain suggests a ruptured viscus. Signs of peritoneal irritation include
abdominal tenderness, rebound tenderness, and abdominal rigidity.
2. In severe cases, fever, hypotension, tachycardia, and acidosis may
occur. Spontaneous bacterial peritonitis arising from ascites will often
present with only subtle signs.
C. Diagnosis
1. Plain abdominal radiographs and a chest x-ray may detect free air
in the abdominal cavity caused by a perforated viscus. CT and/or
ultrasonography can identify the presence of free fluid or an abscess.
2. Paracentesis
a. Tube 1 - Cell count and differential (1-2 mL, EDTA purple top tube)
b. Tube 2 - Gram stain of sediment; C&S, AFB, fungal C&S (3-4 mL);
inject 10-20 mL into anaerobic and aerobic culture bottle at the
bedside.
c. Tube 3 - Glucose, protein, albumin, LDH, triglyceride, specific
gravity, amylase, (2-3 mL, red top tube). Serum/fluid albumin
gradient should be determined.
d. Syringe - pH (3 mL).
D. Treatment of acute peritonitis
1. Resuscitation with intravenous fluids and correction of metabolic and
electrolyte disturbances are the initial steps. Laparotomy is a corner
stone of therapy for secondary or tertiary acute peritonitis.
2. Broad-spectrum systemic antibiotics are critical to cover bowel flora,
including anaerobic species.
3. Mild to moderate infection (community-acquired)
a. Cefotetan (Cefotan) 1-2 gm IV q12h OR
b. Ampicillin/sulbactam (Unasyn) 3.0 gm IV q6h
c. Ticarcillin/clavulanate (Timentin) 3.1 gm IV q6h
4. Severe infection (hospital-acquired)
a. Cefepime (Maxipime) 2 gm IV q12h and metronidazole (Flagyl) 500
mg IV q6h OR
b. Piperacillin/tazobactam (Zosyn) 3.375 gm IV q6h OR
c. Imipenem/cilastatin (Primaxin) 1 g IV q6h OR
94 Peritonitis
d. Ciprofloxacin (Cipro) 400 mg IV q12h and clindamycin 600 mg IV
q8h OR
e. Gentamicin or tobramycin 100-120 mg (1.5 mg/kg); then 80 mg IV
q8h (3-5 mg/kg/d) and metronidazole (Flagyl) 500 mg IV q6h.
II. Spontaneous bacterial peritonitis
A. SBP, which has no obvious precipitating cause, occurs almost exclusively
in cirrhotic patients
B. Diagnosis
1. Spontaneous bacterial peritonitis is diagnosed by paracentesis in
which the ascitic fluid is found to have 250 or more polymorphonuclear
(PMN) cells per cubic millimeter.
C. Therapy
1. Antibiotics are the cornerstone of managing SBP, and laparotomy has
no place in therapy for SBP, unless perforation is present. Three to 5
days of intravenous treatment with broad-spectrum antibiotics is
usually adequate, at which time efficacy can be determined by
estimating the ascitic fluid PMN cell count.
2. Option 1:
a. Cefotaxime (Claforan) 2 gm IV q4-6h
3. Option 2:
a. Ticarcillin/clavulanate (Timentin) 3.1 gm IV q6h OR
b. Piperacillin/tazobactam (Zosyn) 3.375 gm IV q6h or 4.5 gm IV q8h.
4. Option 3 if extended-spectrum beta-lactamase (ESBL):
a. Imipenem/cilastatin (Primaxin) 1.0 gm IV q6h. OR
b. Ciprofloxacin (Cipro) 400 mg IV q12h OR
c. Levofloxacin (Levaquin) 500 mg IV q24h.
References
Drugs for HIV Infection. The Medical letter 2000; 42:1-6.
Preface to the 1997 USPHS/IDSA Guidelines for the Prevention of Opportunistic Infections
in Persons Infected with HIV.
1997 Guidelines for the Use of Antimicrobial Agents in Neutropenic Patients with
Unexplained Fever. Clinical Infectious Diseases 1997; 25:551-73
Hughes W.T. Opportunistic Infections in AIDS Patients. Opportunistic Infections 95:81-93,
1994
Lane HCLaughon B.E. Falloon J., et. al. Recent Advances in the Management of AIDS
related Opportunistic Infections. Ann. Intern. Med. 120:945-955, 1994.
Tunkel A.R, Wispelway B, Scheld W.N: Bacterial meningitis; Recent advances in
pathophysiology and treatment. Ann Int Med 112:610,1990.
Pachon J, et al: Severe community acquired pneumonia. Am Rev Respir Dis 142:36973,
1990
Whittman, DH. Management of Secondary Peritonitis. Annals of Surgery. 1996; 224 (1): 10
18.
Bernard, GR, et al. Efficacy and Safety of Recombinant Human Activated Protein C for
Severe Sepsis. NEJM. 2001; Vol 334, No 10: 699-709.
Gastroenterology
Michael Krutzik, MD
H.L. Daneschvar, MD
S.E. Wilson, MD
Roham T. Zamanian, MD
96 Variceal bleeding
F. Coagulopathy should be assessed and corrected with fresh frozen
plasma, vitamin K, cryoprecipitate, and platelets.
G. Definitive diagnosis requires upper endoscopy, at which time
electrocoagulation, banding, and/or local injection of vasoconstrictors at
bleeding sites may be completed.
H. Surgical consultation should be requested in unstable patients or patients
who require more than 6 units of pRBCs.
VI. Mallory-Weiss syndrome
A. This disorder is defined as a mucosal tear at the gastroesophageal
junction following forceful retching and vomiting.
B. Treatment is supportive, and the majority of patients stop bleeding
spontaneously. Endoscopic coagulation or operative suturing may rarely
be necessary.
VII.
Acute medical treatment of peptic ulcer disease
A. Ranitidine (Zantac) 50 mg IV bolus, then continuous infusion at 6.25-12.5
mg/h [150-300 mg in 250 mL D5W over 24h (11 cc/h)], or 50 mg IV q6-8h
OR
B. Cimetidine (Tagamet) 300 mg IV bolus, then continuous infusion at 37.5
50 mg/h (900 mg in 250 mL D5W over 24h), or 300 mg IV q6-8h OR
C. Famotidine (Pepcid) 20 mg IV q12h.
Variceal Bleeding
Hemorrhage from esophageal and gastric varices usually occurs as a complica
tion of chronic liver disease.
I. Clinical evaluation
A. Variceal bleeding should be considered in any patient who presents with
significant upper gastrointestinal bleeding. Signs of cirrhosis may include
spider angiomas, palmar erythema, leukonychia, clubbing, parotid enlarge
ment, and Dupuytren's contracture. Jaundice, lower extremity edema and
ascites are indicative of decompensated liver disease.
B. The severity of the bleeding episode can be assessed on the basis of
orthostatic changes (eg, resting tachycardia, postural hypotension), which
indicates one-third or more of blood volume loss.
C. If the patient's sensorium is altered because of hepatic encephalopathy, the
risk of aspiration mandates endotracheal intubation. Placement of a large
caliber nasogastric tube (22 F or 24 F) permits lavage for removal of blood
and clots in preparation for endoscopy.
D. Nasogastric lavage should be performed with tap water, because saline
may contribute to retention of sodium and water.
II.
Resuscitation
A. Blood should be replaced as soon as possible. While blood for transfusion
is being made available, intravascular volume should be replenished with
normal saline solution.
B. Once euvolemia is established, the intravenous infusion should be
changed to solutions with a lower sodium content (5% dextrose with or
normal saline).
C. Fresh frozen plasma is administered to patients who have been given
massive transfusions. Each 3 units of PRBC should be accompanied by
CaCL2 1 gm IV over 30 min.
Variceal Bleeding 97
D. Blood should be transfused to maintain a hematocrit of at least 30%. Serial
hematocrit estimations should be obtained during continued bleeding.
III. Treatment of variceal hemorrhage
A. Pharmacologic agents
1. Octreotide (Sandostatin) 50 mcg IV over 5-10 min, followed by 50
mcg/h for 48 hours (1200 mcg in 250 mL D5W). Octreotide is a
somatostatin analog, which is beneficial in controlling hemorrhage.
2. Vasopressin (Pitressin), a posterior pituitary hormone, causes
splanchnic arteriolar vasoconstriction and reduction in portal pressure.
a. Dosage is 20 units IV over 20-30 min, then 0.2-0.4 units/minute (100
U in 250 mL D5W).
b. Concomitant use of IV nitroglycerin paste (1 inch q6h) mitigates the
vasoconstrictor effects of vasopressin on the myocardial and
splanchnic circulations.
B. Tamponade devices
1. Bleeding from varices may temporarily be reduced with tamponade bal
loon tubes. However, the benefit is temporary, and prolonged
tamponade causes severe esophageal ulceration and has a high
rebleeding rate. The Linton-Nachlas tube has a gastric balloon and
several ports in the esophageal component. The tube is kept in place
for 6-12 hours while preparations for endoscopic or radiologic treatment
are being made.
C. Endoscopic management of bleeding varices
1. Endoscopic sclerotherapy involves injection of a sclerosant into
varices. The success of the treatment is enhanced by a second
sclerotherapy treatment.
2. Endoscopic variceal ligation involves placement of tiny rubber bands
on varices during endoscopy. Ligation is associated with fewer
complications than sclerotherapy, but both have comparable efficacy.
D. Surgery
1. Portal-systemic shunt surgery is the most definitive therapy for bleeding
varices. However, the procedures have a 30-40% rate of hepatic
encephalopathy, and there is only a slight survival advantage over
medical treatment.
2. Shunts that preserve portal blood flow are preferred, such as the distal
splenorenal and the small-diameter portacaval H-graft shunts.
E. Transjugular intrahepatic portacaval shunt (TIPS)
1. Under fluoroscopy, a needle is advanced into the liver through the
internal jugular and hepatic veins, and inserted into a large branch of
the portal vein. A balloon is then used to enlarge the track to permit the
placement of a stent.
2. Encephalopathy occurs in about 35% of patients, and there is a
significant risk of shunt thrombosis or stenosis.
IV. Approach to treatment of variceal hemorrhage
A. Patients initially should be given octreotide (Sandostatin) or vasopressin
infusion plus nitroglycerin while awaiting endoscopic treatment.
B. If varices are large, endoscopic ligation is preferred. If there is active bleed
ing from a spurting varix, sclerotherapy is best.
C. Failure of endoscopic therapy warrants the use of a portal-systemic shunt.
Liver transplantation should be considered in poor-risk patients and when
other therapies fail.
Acute Pancreatitis
Blanding U. Jones, MD and Russell A. Williams, MD
The incidence of acute pancreatitis ranges from 54 to 238 episodes per 1 million
per year. Patients with mild pancreatitis respond well to conservative therapy, but
those with severe pancreatitis may have a progressively downhill course to
respiratory failure, sepsis, and death (less than 10%).
I. Etiology
A. Alcohol-induced pancreatitis. Consumption of large quantities of alcohol
may cause acute pancreatitis.
B. Cholelithiasis. Common bile duct or pancreatic duct obstruction by a stone
may cause acute pancreatitis. (90% of all cases of pancreatitis occur
secondary to alcohol consumption or cholelithiasis).
C. Idiopathic pancreatitis. The cause of pancreatitis cannot be determined
in 10 percent of patients.
D. Hypertriglyceridemia. Elevation of serum triglycerides (>l,000mg/dL) has
been linked with acute pancreatitis.
E. Pancreatic duct disruption. In younger patients, a malformation of the
pancreatic ducts (eg, pancreatic divisum) with subsequent obstruction is
often the cause of pancreatitis. In older patients without an apparent
underlying etiology, cancerous lesions of the ampulla of Vater, pancreas or
duodenum must be ruled out as possible causes of obstructive pancreatitis.
F. Iatrogenic pancreatitis. Radiocontrast studies of the hepatobiliary system
(eg, cholangiogram, ERCP) can cause acute pancreatitis in 2-3% of
patients undergoing studies.
G. Trauma. Blunt or penetrating trauma of any kind to the peri-pancreatic or
peri-hepatic regions may induce acute pancreatitis. Extensive surgical
manipulation can also induce pancreatitis during laparotomy.
Causes of Acute Pancreatitis
Alcoholism
Cholelithiasis
Drugs
Hypertriglyceridemia
Idiopathic causes
Infections
Microlithiasis
Pancreas divisum
Trauma
Mercaptopurine (Purinethol)
Pentamidine
Sulfonamides
Tetracyclines
Thiazide diuretics
Valproic acid (Depakote)
Acute alcoholism
Diabetic ketoacidosis
Lung cancer
Ovarian neoplasm
Renal failure
Ruptured ectopic pregnancy
Salivary gland infection
Macroamylasemia
Hepatic Encephalopathy
Hepatic encephalopathy develops when ammonia and toxins, which are usually
metabolized (detoxified) by the liver, enter into the systemic circulation. Hepatic
encephalopathy can be diagnosed in 50-70% of patients with chronic hepatic
failure.
I. Clinical manifestations
A. Hepatic encephalopathy manifests as mild changes in personality to
altered motor functions and/or level of consciousness.
B. Most episodes are precipitated by identifiable factors, including gastroin
testinal bleeding, excessive protein intake, constipation, excessive
diuresis, hypokalemia, hyponatremia or hypernatremia, azotemia,
infection, poor compliance with lactulose therapy, sedatives (benzo
diazepines, barbiturates, antiemetics), hepatic insult (alcohol, drugs, viral
hepatitis), surgery, or hepatocellular carcinoma.
C. Hepatic encephalopathy is a diagnosis of exclusion. Therefore, if a
patient with acute or chronic liver failure suddenly develops altered mental
status, concomitant problems must be excluded, such as intracranial
lesions (hemorrhage, infarct, tumor, abscess), infections (meningitis,
encephalitis, sepsis), metabolic encephalopathies (hyperglycemia or
hypoglycemia, uremia, electrolyte imbalance), alcohol intoxication or
withdrawal, Wernicke's encephalopathy, drug toxicity (sedatives, psycho
active medications), or postictal encephalopathy.
D. Physical exam may reveal hepatosplenomegaly, ascites, jaundice, spider
angiomas, gynecomastia, testicular atrophy, and asterixis.
E. Computed tomography may be useful to exclude intracranial abscess or
hemorrhage. Laboratory evaluation may include serum ammonia, CBC,
electrolyte panel, liver profile, INR/PTT, UA, and blood cultures.
II. Treatment of hepatic encephalopathy
A. Flumazenil (Romazicon) may transiently improve the mental state in
patients with hepatic encephalopathy. Dosage is 0.2 mg (2 mL) IV over 30
seconds q1min until a total dose of 3 mg; if a partial response occurs,
References
Besson I, et al: Sclerotherapy with or without octreotide for acute variceal bleeding, N Eng
J Med 333(9): 555-60, 1995.
Adams L; Soulen MC. TIPS: a New Alternative for the Variceal Bleeder. Am J Crit Care
2:196, 1993.
Grate ND: Diagnosis and treatment of gastrointestinal bleeding secondary to protal
hypertension. AJG 1997; 92(7): 1081-91
Riordan SM; Williams R: Treatment of hepatic encephalopathy. NEJM 1997; 337(7): 473-79
Haber PS; Perola EC; Wilson JS: Clinical update: management of acute pancreatitis. J of
hepatology 1997; 12(3): 189-97
Toxicology
Hans Poggemeyer, MD
Toxicologic Syndromes
I. Characteristics of common toxicologic syndromes
A. Cholinergic poisoning: Salivation, bradycardia, defecation, lacrimation,
emesis, urination, miosis.
B. Anticholinergic poisoning: Dry skin, flushing, fever, urinary retention,
mydriasis, thirst, delirium, conduction delays, tachycardia, ileus.
C. Sympathomimetic poisoning: Agitation, hypertension, seizure,
tachycardia, mydriasis, vasoconstriction.
D. Narcotic poisoning: Lethargy, hypotension, hypoventilation, miosis,
coma, ileus.
E. Withdrawal syndrome: Diarrhea, lacrimation, mydriasis, cramps,
tachycardia, hallucination.
F. Salicylate poisoning: Fever, respiratory alkalosis, or mixed acid-base
disturbance, hyperpnea, hypokalemia, tinnitus.
G. Causes of toxic seizures: Amoxapine, anticholinergics, camphor,
carbon monoxide, cocaine, ergotamine, isoniazid, lead, lindane, lithium,
LSD, parathion, phencyclidine, phenothiazines, propoxyphene
propranolol, strychnine, theophylline, tricyclic antidepressants,
normeperidine (metabolite of meperidine), thiocyanate.
H. Causes of toxic cardiac arrhythmias: Arsenic, beta-blockers, chloral
hydrate, chloroquine, clonidine, calcium channel blockers, cocaine,
cyanide, carbon monoxide, digitalis, ethanol, phenol, phenothiazine,
tricyclics.
I. Extrapyramidal syndromes: Dysphagia, dysphonia, trismus, rigidity,
torticollis, laryngospasm.
Acetaminophen Overdose
I. Clinical features
A. Acute lethal dose = 13-25 g. Acetaminophen is partly metabolized to
N-acetyl-p-benzoquinonimine which is conjugated by glutathione. Hepatic
glutathione stores can be depleted in acetaminophen overdose, leading to
centrilobular hepatic necrosis.
B. Liver failure occurs 3 days after ingestion if untreated. Liver failure
presents with right upper quadrant pain, elevated liver function tests,
coagulopathy, hypoglycemia, renal failure and encephalopathy.
II. Treatment
A. Gastrointestinal decontamination should consist of gastric lavage
followed by activated charcoal. Residual charcoal should be removed with
saline lavage prior to giving N-acetyl-cysteine (NAC).
I NT E R P RE T A T IO N O F AC TA M I N O P HE N L E V E L
V S H O UR S P O S T I N G E S TI O N
3 00
2 50
2 00
1 50
1 00
90
80
70
60
50
40
30
20
10
9
8
7
6
5
4
3
2
1
5
10
15
20
25
30
H ou rs P os t In ges t io n
N o ri sk o f tox ic ity if u n d e r d o u b le l in e s.
P ro b a b le ri sk if a b o ve to p li n e .
P o ss ib l e r is k i f b etw e e n d o u bl e li n e s.
i ng e s tio n .
G r a p h a p p l ie s to n o n -s u sta in e d re l e a se fo rm u l ati o n s o n ly .
35
Cocaine Overdose
I. Clinical evaluation
A. Cocaine can be used intravenously, smoked, ingested, or inhaled nasally.
Street cocaine often is cut with other substances including amphetamines,
LSD, PCP, heroin, strychnine, lidocaine, talc, and quinine.
B. One-third of fatalities occur within 1 hour, with another third occurring 6-24
hours later.
C. Persons may transport cocaine by swallowing wrapped packets, and some
users may hastily swallow packets of cocaine to avoid arrest.
II. Clinical features
A. CNS: Sympathetic stimulation, agitation, seizures, tremor, headache,
subarachnoid hemorrhage, ischemic cerebral stoke, psychosis, hallucina
tions, fever, mydriasis, formication (sensation of insects crawling on skin).
B. Cardiovascular: Atrial and ventricular arrhythmias, myocardial infarction,
hypertension, hypotension, myocarditis, aortic rupture, cardiomyopathy.
C. Pulmonary: Noncardiogenic pulmonary edema, pneumomediastinum,
alveolar hemorrhage, hypersensitivity pneumonitis, bronchiolitis obliterans.
D. Other: Rhabdomyolysis, mesenteric ischemia, hepatitis.
III. Treatment
A. Treatment consists of supportive care because no antidote exists. GI
decontamination, including repeated activated charcoal, whole bowel
irrigation and endoscopic evaluation is provided if oral ingestion is
suspected.
B. Hyperadrenergic symptoms should be treated with benzodiazepines, such
as lorazepam.
C. Seizures: Treat with lorazepam, phenytoin, or phenobarbital.
D. Arrhythmias
1. Treat hyperadrenergic state and supraventricular tachycardia with
lorazepam and propranolol.
2. Ventricular arrhythmias are treated with lidocaine or propranolol.
E. Hypertension
1. Use lorazepam first for tachycardia and hypertension.
2. If no response, use labetalol because it has alpha and beta blocking
effects.
3. If hypertension remains severe, administer sodium nitroprusside or
esmolol drip.
F. Myocardial ischemia and infarction: Treat with thrombolysis, heparin,
aspirin, beta-blockers, nitroglycerin. Control hypertension and exclude
CNS bleeding before using thrombolytic therapy.
Digoxin Overdose
I. Clinical features
A. The therapeutic window of digoxin is 0.8-2.0 ng/mL. Drugs that increase
digoxin levels include verapamil, quinidine, amiodarone, flecainide,
erythromycin, and tetracycline. Hypokalemia, hypomagnesemia and
hypercalcemia enhance digoxin toxicity.
B. CNS: Confusion, lethargy; yellow-green visual halo.
C. Cardiac: Common dysrhythmias include ventricular tachycardia or
fibrillation; variable atrioventricular block, atrioventricular dissociation;
sinus bradycardia, junctional tachycardia, premature ventricular contrac
tions.
D. GI: Nausea, vomiting.
Gamma-hydroxybutyrate Ingestion
I. Clinical features
A. Gamma-hydroxybutyrate (GHB) was used as an anesthetic agent but was
banned because of the occurrence of seizures. Gamma-hydroxybutyrate
is now an abused substance at dance clubs because of the euphoric
effects of the drug. It is also abused by body builders because of a
mistaken belief that it has anabolic properties. Gamma-hydroxybutyrate
is a clear, odorless, oily, salty liquid. It is rapidly absorbed within 20-40
minutes of ingestion and metabolized in the liver. The half-life of GHB is
20-30 min.
B. Gamma-hydroxybutyrate is not routinely included on toxicological
screens, but it can be detected in the blood and urine by gas chromatog
raphy within 12 hours of ingestion. Gamma hydroxybutyrate may cause
respiratory depression, coma, seizures, and severe agitation. Cardiac
effects include hypotension, cardiac arrest, and severe vomiting.
II. Treatment
A. Gastric lavage is not indicated due to rapid absorption of GHB.
B. Immediate care consists of support of ventilation and circulation.
Agitation should be treated with benzodiazepines, haloperidol, or
propofol. Seizures should be treated with lorazepam, phenytoin, or
valproic acid.
Iron Overdose
I. Clinical features
A. Toxicity is caused by free radical organ damage to the GI mucosa, liver,
kidney, heart, and lungs. The cause of death is usually shock and liver
failure.
Toxic dosages and serum levels
Nontoxic
Toxic
Lethal
Lithium Overdose
I. Clinical features
A. Lithium has a narrow therapeutic window of 0.8-1.2 mEq/L.
B. Drugs that will increase lithium level include NSAIDs, phenothiazines,
thiazide and loop diuretics (by causing hyponatremia).
C. Toxicity
1.5-3.0 mEq/L = moderate toxicity
3.0-4.0 mEq/L = severe toxicity
D. Toxicity in chronic lithium users occurs at much lower serum levels than
with acute ingestions.
E. Common manifestations include seizures, encephalopathy, hyperreflexia,
tremor, nausea, vomiting, diarrhea, hypotension. Nephrogenic diabetes
insipidus and hypothyroidism may also occur. Conduction block and
dysrhythmias are rare, but reversible T-wave depression may occur.
II. Treatment
A. Correct hyponatremia with aggressive normal saline hydration. Follow
lithium levels until <1.0 mEq/L.
Methanol Ingestion
I. Clinical features
A. Methanol is found in antifreeze, Sterno, cleaners, and paints.
B. Toxicity
1. 10 cc causes blindness
2. Minimal lethal dose = 1-5 g/kg
3. Lethal blood level = 80 mg/dL
4. Symptomatic in 40 minutes to 72 hours.
C. Signs and Symptoms
1. Severe osmolar and anion gap metabolic acidosis.
2. Visual changes occur because of optic nerve toxicity, leading to
blindness.
3. Nausea, vomiting, abdominal pain, pancreatitis, and altered mental
status.
II. Treatment
A. Ethanol 10% is infuse in D5W as 7.5 cc/kg load then 1.4 cc/kg/h drip to
keep blood alcohol level between 100-150 mg/dL. Continue therapy until
the methanol level is below 20-25 mg/dL.
B. Give folate 50 mg IV q4h to enhance formic acid metabolism.
C. Correct acidosis and electrolyte imbalances.
D. Hemodialysis: Indications: peak methanol level >50 mg/dL; formic acid
level >20 mg/dL; severe metabolic acidosis; acute renal failure; any visual
compromise.
Salicylate Overdose
I. Clinical features
A. Toxicity
150-300 mg/kg - mild toxicity
300-500 mg/kg - moderate toxicity
>500 mg/kg - severe toxicity
B. Chronic use can cause toxicity at much lower levels (ie, 25 mg/dL) than
occurs with acute use.
C. Acid/Base Abnormalities: Patients present initially with a respiratory
alkalosis because of central hyperventilation. Later an anion gap metabolic
acidosis occurs.
D. CNS: Tinnitus, lethargy, irritability, seizures, coma, cerebral edema.
E. GI: Nausea, vomiting, liver failure, GI bleeding.
Theophylline Toxicity
I. Clinical features
A. Drug interactions can increase serum theophylline level, including
quinolone and macrolide antibiotics, propranolol, cimetidine, and oral
contraceptives. Liver disease or heart failure will decrease clearance.
B. Serum toxicity levels
20-40 mg/dL - mild
40-70 mg/dL - moderate
>70 mg/dL - life threatening
C. Toxicity in chronic users occurs at lower serum levels than with short-term
users. Seizures and arrhythmias can occur at therapeutic or minimally
supra-therapeutic levels.
D. CNS: Hyperventilation, agitation, and tonic-clonic seizures.
E. Cardiac: Sinus tachycardia, multi-focal atrial tachycardia, supraventricular
tachycardia, ventricular tachycardia and fibrillation, premature ventricular
contractions, hypotension or hypertension.
F. Gastrointestinal: Vomiting, diarrhea, hematemesis.
G. Musculoskeletal: Tremor, myoclonic jerks
H. Metabolic: Hypokalemia, hypomagnesemia, hypophosphatemia, hyper
glycemia, and hypercalcemia.
II. Treatment
A. Gastrointestinal decontamination and systemic drug removal
1. Activated charcoal premixed with sorbitol, 50 gm PO or via nasogastric
tube q4h around-the-clock until theophylline level is less than 20
mcg/mL. Maintain head-of-bed at 30 degrees to prevent charcoal
aspiration.
Neurologic Disorders
Hans Poggemeyer, MD
Ischemic Stroke
Ischemic stroke is the third leading cause of death in the United States and the
most common cause of neurologic disability in adults. Approximately 85 percent
of strokes are ischemic in nature.
I.
Space-occupying lesions
Intracerebral hemorrhage
Epidural hemorrhage
Subdural hemorrhage
Tumor
Abscess
Hydrocephalus
Subarachnoid hemorrhage
Meningitis
Aqueductal stenosis
Idiopathic
Miscellaneous
Pseudotumor cerebri
Craniosynostosis
Venous sinus thrombosis
Dose
Advantages
Limitations
Mannitol 0.5 to 1 R a p i d
o n s e t , H y pote n s i on, hypo
g/kg IV push
titratable, predictable kalemia, duration hours or
days
Barbiturates
Status Epilepticus
Status epilepticus (SE) is defined as a continuous seizures lasting at least 5
minutes, or 2 or more discrete seizures between which there is incomplete
recovery of consciousness. Simple seizures are characterized by focal motor or
sensory phenomena, with full preservation of consciousness. Generalized
seizures include generalized tonic-clonic seizures. Complex seizures are
diagnosed when an alteration in consciousness has occurred.
I. Diagnostic evaluation
A. Laboratory evaluation
1. CBC, blood glucose level, serum electrolytes (sodium, magnesium,
calcium), anticonvulsant drug levels, and urinalysis.
2. Lumbar puncture is necessary if meningitis or subarachnoid hemor
rhage is suspected.
3. Toxicologic screening is indicated in specific situations.
B. CT scan is indicated if tumor, abscess, subarachnoid hemorrhage, or
trauma is suspected, or if the patient has no prior history of seizures.
C. Electroencephalogram. An immediate EEG may be required if the patient
fails to awaken promptly after the seizure.
Etiology of Status Epilepticus
Status epilepticus in a patient with a history of seizure disorder
Noncompliance with prescribed medical regimen
Withdrawal seizures from anticonvulsants
Breakthrough seizures
New onset seizure disorder presenting with status epilepticus
Status epilepticus secondary to medical, toxicologic, or structural
symptoms
Anoxic brain injury
Stroke syndromes
Subarachnoid hemorrhage
Intracranial tumor
Trauma
Theophylline, cocaine, amphetamine or isoniazid overdose; alcohol
withdrawal, gamma hydroxybutyrate
Hyponatremia, hypernatremia, hypercalcemia, hypomagnesemia,
hepatic encephalopathy
Meningitis, brain abscess, encephalitis, CNS cysticercosis or
toxoplasmosis
II. Management of generalized convulsive status epilepticus (GCSE)
A. A history should be obtained, and a brief physical examination per
formed. Initial stabilization consists of airway management, 100%
oxygen by mask, rapid glucose testing, intravenous access, and cardiac
and hemodynamic monitoring.
Endocrinologic
Disorders
and
Nephrologic
Michael Krutzik, MD
Guy Foster, MD
Diabetic Ketoacidosis
Diabetic ketoacidosis is defined by hyperglycemia, metabolic acidosis, and
ketosis.
I. Clinical presentation
A. Diabetes is newly diagnosed in 20% of cases of diabetic ketoacidosis. In
patients with known diabetes, precipitating factors include infection,
noncompliance with insulin, myocardial infarction, and gastrointestinal
bleeding.
B. Symptoms of DKA include polyuria, polydipsia, fatigue, nausea, and
vomiting, developing over 1 to 2 days. Abdominal pain is prominent in
25%.
C. Physical examination
1. Patients are typically flushed, tachycardic, tachypneic, and volume
depleted with dry mucous membranes. Kussmaul's respiration (rapid,
deep breathing and air hunger) occurs when the serum pH is between
7.0 and 7.24.
2. A fruity odor on the breath indicates the presence of acetone, a
byproduct of diabetic ketoacidosis.
3. Fever, although seldom present, indicates infection. Eighty percent of
patients with diabetic ketoacidosis have altered mental status. Most
are awake but confused; 10% are comatose.
D. Laboratory findings
1. Serum glucose level >300 mg/dL
2. pH <7.35, pCO2 <40 mm Hg
3. Bicarbonate level below normal with an elevated anion gap
4. Presence of ketones in the serum
II. Differential diagnosis
A. Differential diagnosis of ketosis-causing conditions
1. Alcoholic ketoacidosis occurs with heavy drinking and vomiting. It
does not cause an elevated glucose.
2. Starvation ketosis occurs after 24 hours without food and is not
usually confused with DKA because glucose and serum pH are
normal.
B. Differential diagnosis of acidosis-causing conditions
1. Metabolic acidoses are divided into increased anion gap (>14
mEq/L) and normal anion gap; anion gap = sodium - (CI- + HCO3-).
2. Anion gap acidoses can be caused by ketoacidoses, lactic acidosis,
uremia, salicylate, methanol, ethanol, or ethylene glycol poisoning.
3. Non-anion gap acidoses are associated with a normal glucose level
and absent serum ketones. Causes of non-anion gap acidoses
include renal or gastrointestinal bicarbonate loss.
Monitoring of therapy
B.
C.
III.
A.
B.
C.
D.
Hyperkalemia 133
B. Extracellular fluid volume expansion. Infusion of a 1-2 liter crystalloid
fluid bolus may confirm suspected volume depletion.
C. If the patient remains oliguric despite euvolemia, IV diuretics may be
administered. A large single dose of furosemide (100-200 mg) may be
administered intravenously to promote diuresis. If urine flow is not
improved, the dose of furosemide may be doubled. Furosemide may be
repeated in 2 hours, or a continuous IV infusion of 10-40 mg/hr (max 1000
mg/day) may be used.
D. The dosage or dosing intervals of renally excreted drugs should be
modified.
E. Hyperkalemia is the most immediately life-threatening complication of
renal failure. Serum potassium values greater than 6.5 mEq/L may lead to
arrhythmias and cardiac arrest. Potassium should be removed from IV
solutions. Hyperkalemia may be treated with sodium polystyrene sulfonate
(Kayexalate), 30-60 gm PO/PR every 4-6 hours.
F. Hyperphosphatemia can be controlled with aluminum hydroxide antacids
(eg, Amphojel or Basaljel), 15-30 ml or one to three capsules PO with
meals, should be used.
G. Fluids. After normal volume has been restored, fluid intake should be
reduced to an amount equal to urinary and other losses plus insensible
losses of 300-500 mL/day. In oliguric patients, daily fluid intake may need
to be restricted to less than 1 L.
H. Nutritional therapy. A renal diet consisting of daily high biologic value
protein intake of 0.5 gm/kg/d, sodium 2 g, potassium 40-60 mg/day, and
at least 35 kcal/kg of nonprotein calories is recommended. Phosphorus
should be restricted to 800 mg/day
I. Dialysis. Indications for dialysis include uremic pericarditis, severe
hyperkalemia, pulmonary edema, persistent severe metabolic acidosis (pH
less than 7.2), and symptomatic uremia.
Hyperkalemia
Body potassium is 98% intracellular. Only 2% of total body potassium, about 70
mEq, is in the extracellular fluid, with the normal concentration of 3.5-5 mEq/L.
I.
134 Hyperkalemia
III.
IV.
V.
VI.
Hyperkalemia 135
C. High urinary K, excretion of >20 mEq/day, is indicative of excessive K
intake as the cause.
VII.
Renal hyperkalemia
A. If urinary K excretion is low and urine output is in the oliguric range, and
creatinine clearance is lower than 20 cc/minute, renal failure is the
probable cause. Prerenal azotemia resulting from volume depletion must
be ruled out because the hyperkalemia will respond to volume restoration.
B. When urinary K excretion is low, yet blood urea nitrogen and creatinine
levels are not elevated and urine volume is at least 1 L daily and renal
sodium excretion is adequate (about 20 mEq/day), then either a defect in
the secretion of renin or aldosterone or tubular resistance to aldosterone
is likely. Low plasma renin and aldosterone levels, will confirm the
diagnosis of hyporeninemic hypoaldosteronism. Addison's disease is
suggested by a low serum cortisol, and the diagnosis is confirmed with a
ACTH (Cortrosyn) stimulation test.
C. When inadequate K excretion is not caused by hypoaldosteronism, a
tubular defect in K clearance is suggested. Urinary tract obstruction, renal
transplant, lupus, or a medication should be considered.
VIII. Extrarenal hyperkalemia
A. When hyperkalemia occurs along with high urinary K excretion of >20
mEq/day, excessive intake of K is the cause. Potassium excess in IV
fluids, diet, or medication should be sought. A concomitant underlying
renal defect in K excretion is also likely to be present.
B. Blood sugar should be measured to rule out insulin deficiency; blood pH
and serum bicarbonate should be measured to rule out acidosis.
C. Endogenous sources of K, such as tissue necrosis, hypercatabolism,
hematoma, gastrointestinal bleeding, or intravascular hemolysis should
be excluded.
IX. Management of hyperkalemia
A. Acute treatment of hyperkalemia
1. Calcium
a. If the electrocardiogram shows loss of P waves or widening of QRS
complexes, calcium should be given IV; calcium reduces the cell
membrane threshold potential.
b. Calcium chloride (10%) 2-3 g should be given over 5 minutes. In
patients with circulatory compromise, 1 g of calcium chloride IV
should be given over 3 minutes.
c. If the serum K level is greater than 7 mEq/L, calcium should be
given. If digitalis intoxication is suspected, calcium must be given
cautiously. Coexisting hyponatremia should be treated with
hypertonic saline.
2. Insulin: If the only ECG abnormalities are peaked T waves and the
serum level is under 7 mEq/L, treatment should begin with insulin
(regular insulin, 5-10 U by IV push) with 50% dextrose water (D50W)
50 mL IV push. Repeated insulin doses of 10 U and glucose can be
given every 15 minutes for maximal effect.
3. Sodium bicarbonate promotes cellular uptake of K. It should be given
as 1-2 vials (50-mEq/vials) IV push.
4. Potassium elimination measures
a. Sodium polystyrene sulfonate (Kayexalate) is a cation exchange
resin which binds to potassium in the lower GI tract. Dosage is 30
60 gm premixed with sorbitol 20% PO/PR.
136 Hypokalemia
b. Furosemide (Lasix) 100 mg IV should be given to promote
kaliuresis.
c. Emergent hemodialysis for hyperkalemia is rarely necessary except
when refractory metabolic acidosis is present.
Hypokalemia
Hypokalemia is characterized by a serum potassium concentration of less than
3.5 mEq/L. Ninety-eight percent of K is intracellular.
I. Pathophysiology of hypokalemia
A. Cellular redistribution of potassium. Hypokalemia may result from the
intracellular shift of potassium by insulin, beta-2 agonist drugs, stress
induced catecholamine release, thyrotoxic periodic paralysis, and
alkalosis-induced shift (metabolic or respiratory).
B. Nonrenal potassium loss
1. Gastrointestinal loss can be caused by diarrhea, laxative abuse,
villous adenoma, biliary drainage, enteric fistula, clay ingestion,
potassium binding resin ingestion, or nasogastric suction.
2. Sweating, prolonged low-potassium diet, hemodialysis and peritoneal
dialysis may also cause nonrenal potassium loss.
C. Renal potassium loss
1. Hypertensive high renin states. Malignant hypertension, renal artery
stenosis, renin-producing tumors.
2. Hypertensive low renin, high aldosterone states. Primary
hyperaldosteronism (adenoma or hyperplasia).
3. Hypertensive low renin, low aldosterone states. Congenital adrenal
hyperplasia (11 or 17 hydroxylase deficiency), Cushing's syndrome or
disease, exogenous mineralocorticoids (Florinef, licorice, chewing
tobacco), Liddle's syndrome.
4. Normotensive states
a. Metabolic acidosis. Renal tubular acidosis (type I or II)
b. Metabolic alkalosis (urine chloride <10 mEq/day). Vomiting
c. Metabolic alkalosis (urine chloride >10 mEq/day). Bartter's
syndrome, diuretics, magnesium depletion, normotensive hyper
aldosteronism
5. Drugs associated with potassium loss include amphotericin B,
ticarcillin, piperacillin, and loop diuretics.
II. Clinical effects of hypokalemia
A. Cardiac effects. The most lethal consequence of hypokalemia is cardiac
arrhythmia. Electrocardiographic effects include a depressed ST seg
ment, decreased T-wave amplitude, U waves, and a prolonged QT-U
interval.
B. Musculoskeletal effects. The initial manifestation of K depletion is
muscle weakness, which can lead to paralysis. In severe cases,
respiratory muscle paralysis may occur.
C. Gastrointestinal effects. Nausea, vomiting, constipation, and paralytic
ileus may develop.
III. Diagnostic evaluation
Hypermagnesemia 137
A. The 24-hour urinary potassium excretion should be measured. If >20
mEq/day, excessive urinary K loss is the cause. If <20 mEq/d, low K
intake, or non-urinary K loss is the cause.
B. In patients with excessive renal K loss and hypertension, plasma renin
and aldosterone should be measured to differentiate adrenal from non
adrenal causes of hyperaldosteronism.
C. If hypertension is absent and serum pH is acidotic, renal tubular acidosis
should be considered. If hypertension is absent and serum pH is normal
to alkalotic, a high urine chloride (>10 mEq/d) suggests hypokalemia
secondary to diuretics or Bartter's syndrome. A low urine chloride (<10
mEq/d) suggests vomiting.
IV.
Emergency treatment of hypokalemia
A. Indications for urgent replacement. Electrocardiographic abnormalities,
myocardial infarction, hypoxia, digitalis intoxication, marked muscle
weakness, or respiratory muscle paralysis.
B. Intravenous potassium therapy
1. Intravenous KCL is usually used unless concomitant hypo
phosphatemia is present, where potassium phosphate is indicated.
2. The maximal rate of intravenous K replacement is 30 mEq/hour. The
K concentration of IV fluids should be 80 mEq/L or less if given via a
peripheral vein. Frequent monitoring of serum K and constant
electrocardiographic monitoring is recommended when potassium
levels are being replaced.
V. Non-emergent treatment of hypokalemia
A. Attempts should be made to normalize K levels if <3.5 mEq/L.
B. Oral supplementation is significantly safer than IV. Liquid formulations are
preferred due to rapid oral absorption, compared to sustained release
formulations, which are absorbed over several hours.
1. KCL elixir 20-40 mEq qd-tid PO after meals.
2. Micro-K, 10 mEq tabs, 2-3 tabs tid PO after meals (40-100 mEq/d).
Hypomagnesemia
Magnesium deficiency occurs in up to 11% of hospitalized patients. The normal
range of serum magnesium is 1.5 to 2.0 mEq/L, which is maintained by the
kidney, intestine, and bone.
I. Pathophysiology
A. Decreased magnesium intake. Protein-calorie malnutrition, prolonged
parenteral fluid administration, and catabolic illness are common causes
of hypomagnesemia.
B. Gastrointestinal losses of magnesium may result from prolonged
nasogastric suction, laxative abuse, and pancreatitis.
C. Renal losses of magnesium
1. Renal loss of magnesium may occur secondary to renal tubular
acidosis, glomerulonephritis, interstitial nephritis, or acute tubular
necrosis.
2. Hyperthyroidism, hypercalcemia, and hypophosphatemia may cause
magnesium loss.
138 Hypermagnesemia
3. Agents that enhance renal magnesium excretion include alcohol,
loop and thiazide diuretics, amphotericin B, aminoglycosides, cisplatin,
and pentamidine.
D. Alterations in magnesium distribution
1. Redistribution of circulating magnesium occurs by extracellular to
intracellular shifts, sequestration, hungry bone syndrome, or by acute
administration of glucose, insulin, or amino acids.
2. Magnesium depletion can be caused by large quantities of parenteral
fluids and pancreatitis-induced sequestration of magnesium.
II. Clinical manifestations of hypomagnesemia
A. Neuromuscular findings may include positive Chvostek's and Trous
seau's signs, tremors, myoclonic jerks, seizures, and coma.
B. Cardiovascular. Ventricular tachycardia, ventricular fibrillation, atrial
fibrillation, multifocal atrial tachycardia, ventricular ectopic beats, hyper
tension, enhancement of digoxin-induced dysrhythmias, and cardio
myopathies.
C. ECG changes include ventricular arrhythmias (extrasystoles, tachycardia)
and atrial arrhythmias (atrial fibrillation, supraventricular tachycardia,
torsades de Pointes). Prolonged PR and QT intervals, ST segment
depression, T-wave inversions, wide QRS complexes, and tall T-waves
may occur.
III. Clinical evaluation
A. Hypomagnesemia is diagnosed when the serum magnesium is less than
0.7-0.8 mmol/L. Symptoms of magnesium deficiency occur when the
serum magnesium concentration is less than 0.5 mmol/L. A 24-hour urine
collection for magnesium is the first step in the evaluation of
hypomagnesemia. Hypomagnesia caused by renal magnesium loss is
associated with magnesium excretion that exceeds 24 mg/day.
B. Low urinary magnesium excretion (<1 mmol/day), with concomitant serum
hypomagnesemia, suggests magnesium deficiency due to decreased
intake, nonrenal losses, or redistribution of magnesium.
IV.
Treatment of hypomagnesemia
A. Asymptomatic magnesium deficiency
1. In hospitalized patients, the daily magnesium requirements can be
provided through either a balanced diet, as oral magnesium supple
ments (0.36-0.46 mEq/kg/day), or 16-30 mEq/day in a parenteral
nutrition formulation.
2. Magnesium oxide is better absorbed and less likely to cause diarrhea
than magnesium sulfate. Magnesium oxide preparations include MagOx 400 (240 mg elemental magnesium per 400 mg tablet), Uro-Mag
(84 mg elemental magnesium per 400 mg tablet), and magnesium
chloride (Slo-Mag) 64 mg/tab, 1-2 tabs bid.
B. Symptomatic magnesium deficiency
1. Serum magnesium #0.5 mmol/L requires IV magnesium repletion with
electrocardiographic and respiratory monitoring.
2. Magnesium sulfate 1-6 gm in 500 mL of D5W can be infused IV at 1
gm/hr. An additional 6-9 gm of MgSO4 should be given by continuous
infusion over the next 24 hours.
Hypermagnesemia 139
Hypermagnesemia
Serum magnesium has a normal range of 0.8-1.2 mmol/L. Magnesium
homeostasis is regulated by renal and gastrointestinal mechanisms.
Hypermagnesemia is usually iatrogenic and is frequently seen in conjunction with
renal insufficiency.
I. Clinical evaluation of hypermagnesemia
A. Causes of hypermagnesemia
1. Renal. Creatinine clearance <30 mL/minute.
2. Nonrenal. Excessive use of magnesium cathartics, especially with
renal failure; iatrogenic overtreatment with magnesium sulfate.
B. Cardiovascular manifestations of hypermagnesemia
1. Hypermagnesemia <10 mEq/L. Delayed interventricular conduction,
first-degree heart block, prolongation of the Q-T interval.
2. Levels greater than 10 mEq/L. Low-grade heart block progressing
to complete heart block and asystole occurs at levels greater than
12.5 mmol/L (>6.25 mmol/L).
C. Neuromuscular effects
1. Hyporeflexia occurs at a magnesium level >4 mEq/L (>2 mmol/L);
diminution of deep tendon reflexes is an early sign of magnesium
toxicity.
2. Respiratory depression due to respiratory muscle paralysis, somno
lence and coma occur at levels >13 mEq/L (6.5 mmol/L).
3. Hypermagnesemia should always be considered when these
symptoms occur in patients with renal failure, in those receiving
therapeutic magnesium, and in laxative abuse.
II. Treatment of hypermagnesemia
A. Asymptomatic, hemodynamically stable patients. Moderate hyper
magnesemia can be managed by elimination of intake.
B. Severe hypermagnesemia
1. Furosemide 20-40 mg IV q3-4h should be given as needed. Saline
diuresis should be initiated with 0.9% saline, infused at 120 cc/h to
replace urine loss.
2. If ECG abnormalities (peaked T waves, loss of P waves, or widened
QRS complexes) or if respiratory depression is present, IV calcium
gluconate should be given as 1-3 ampules (10% solution, 1 gm per 10
mL amp), added to saline infusate. Calcium gluconate can be infused
to reverse acute cardiovascular toxicity or respiratory failure as 15
mg/kg over a 4-hour period.
3. Parenteral insulin and glucose can be given to shift magnesium into
cells. Dialysis is necessary for patients who have severe
hypermagnesemia.
Isoproterenol
Prostaglandin E1
Meperidine
Nicotine
Tolbutamide
Vincristine
Tolazamide
Glyburide
Amphotericin B
Colchicine
Vinblastine
C. Diagnosis of hypernatremia
1. Assessment of urine volume and osmolality are essential in the
evaluation of hyperosmolality. The usual renal response to
hypernatremia is the excretion of the minimum volume (#500 mL/day)
of maximally concentrated urine (urine osmolality >800 mOsm/kg).
These findings suggest extrarenal water loss.
2. Diabetes insipidus generally presents with polyuria and hypotonic
urine (urine osmolality <250 mOsm/kg).
V. Management of hypernatremia
A. If there is evidence of hemodynamic compromise (eg, orthostatic
hypotension, marked oliguria), fluid deficits should be corrected initially
with isotonic saline. Once hemodynamic stability is achieved, the
remaining free water deficit should be corrected with 5% dextrose water
or 0.45% NaCl.
B. The water deficit can be estimated using the following formula:
Water deficit = 0.6 x wt in kg x (1 - [140/measured sodium]).
C. The change in sodium concentration should not exceed 1 mEq/liter/hour.
One-half of the calculated water deficit can be administered in the first 24
hours, followed by correction of the remaining deficit over the next 1-2
days. The serum sodium concentration and ECF volume status should be
evaluated every 6 hours. Excessively rapid correction of hypernatremia
may lead to lethargy and seizures secondary to cerebral edema.
D. Maintenance fluid needs from ongoing renal and insensible losses must
also be provided. If the patient is conscious and able to drink, water
should be given orally or by nasogastric tube.
E. Treatment of diabetes insipidus
1. Vasopressin (Pitressin) 5-10 U IV/SQ q6h; fast onset of action with
short duration.
2. Desmopressin (DDAVP) 2-4 mcg IV/SQ q12h; slow onset of action
with long duration of effect.
VI.
Mixed disorders
A. Water excess and saline deficit occurs when severe vomiting and
diarrhea occur in a patient who is given only water. Clinical signs of
volume contraction and a low serum sodium are present. Saline deficit is
replaced and free water intake restricted until the serum sodium level has
normalized.
B. Water and saline excess often occurs with heart failure, manifesting as
edema and a low serum sodium. An increase in the extracellular fluid
volume, as evidenced by edema, is a saline excess. A marked excess of
free water expands the extracellular fluid volume, causing apparent
hyponatremia. However, the important derangement in edema is an
excess of sodium. Sodium and water restriction and use of furosemide
are usually indicated in addition to treatment of the underlying disorder.
Hypercalcemic Crisis
Hypercalcemic crisis is defined as an elevation in serum calcium that is
associated with volume depletion, mental status changes, and life-threatening
cardiac arrhythmias. Hypercalcemic crisis is most commonly caused by
malignancy-associated bone resorption.
I. Diagnosis
A. Hypercalcemic crisis is often complicated by nausea, vomiting,
hypovolemia, mental status changes, and hypotension.
B. A correction for the low albumin level must be made because ionized
calcium is the physiologically important form of calcium.
Corrected serum calcium (mg/dL) = serum calcium + 0.8 x (4.0 - albumin
[g/dL])
C. Most patients in hypercalcemic crisis have a corrected serum calcium
level greater than 13 mg/dL.
D. The ECG often demonstrates a short QT interval. Bradyarrhythmias, heart
blocks, and cardiac arrest may also occur.
II. Treatment of hypercalcemic crisis
A. Normal saline should be administered until the patient is normovolemic.
If signs of fluid overload develop, furosemide (Lasix) can be given to pro
mote sodium and calcium diuresis. Thiazide diuretics, vitamin D
supplements and antacids containing sodium bicarbonate should be
discontinued.
B. Pamidronate disodium (Aredia) is the agent of choice for long-term
treatment of hypercalcemia. A single dose of 90-mg infused IV over 24
hours should normalize calcium levels in 4 to 7 days. The pamidronate
dose of 30- to 90-mg IV infusion may be repeated 7 days after the initial
dose. Smaller doses (30 or 60 mg IV over 4 hours) are given every few
weeks to maintain normal calcium levels.
C. Calcitonin (Calcimar, Miacalcin) has the advantage of decreasing serum
calcium levels within hours; 4 to 8 U/kg SQ/IM q12h. Calcitonin should be
used in conjunction with pamidronate in severely hypercalcemic patients.
144 Hypophosphatemia
Hypophosphatemia
Clinical manifestations of hypophosphatemia include heart failure, muscle
weakness, tremor, ataxia, seizures, coma, respiratory failure, delayed weaning
from ventilator, hemolysis, and rhabdomyolysis.
I.
Hyperphosphatemia 145
A. Increased urinary excretion: Hyperparathyroidism, renal tubular defects,
diuretics.
B. Decrease in GI absorption: Malnutrition, malabsorption, phosphate
binding minerals (aluminum-containing antacids).
C. Abnormal vitamin D metabolism: Vitamin D deficiency, familial hypo
phosphatemia, tumor-associated hypercalcemia.
D. Intracellular shifts of phosphate: Diabetic ketoacidosis, respiratory
alkalosis, alcohol withdrawal, recovery phase of starvation.
II. Labs: Phosphate, SMA 12, LDH, magnesium, calcium, albumin, PTH, urine
electrolytes. 24-hr urine phosphate, and creatinine.
III. Diagnostic approach to hypophosphatemia
A. 24-hr urine phosphate
1. If 24-hour urine phosphate is less than 100 mg/day, the cause is
gastrointestinal losses (emesis, diarrhea, NG suction, phosphate
binders), vitamin D deficit, refeeding, recovery from burns, alkalosis,
alcoholism, or DKA.
2. If 24-hour urine phosphate is greater than 100 mg/day, the cause is
renal losses, hyperparathyroidism, hypomagnesemia, hypokalemia,
acidosis, diuresis, renal tubular defects, or vitamin D deficiency.
IV. Treatment
A. Mild hypophosphatemia (1.0-2.5 mEq/dL)
1. Na or K phosphate 0.25 mMol/kg IV infusion at the rate of 10 mMol/hr
(in NS or D5W 150-250 mL), may repeat as needed.
2. Neutral phosphate (Nutra-Phos), 2 packs PO bid-tid (250 mg
elemental phosphorus/pack.
B. Severe hypophosphatemia (<1.0 mEq/dL)
1. Administer Na or K phosphate 0.5 m Moles/Kg IV infusion at the rate
of 10 mMoles/hr (NS or D5W 150-250 mL), may repeat as needed.
2. Add potassium phosphate to IV solution in place of KCl (max 80
mEq/L infused at 100-150 mL/h). Max IV dose 7.5 mg phospho
rus/kg/6h OR 2.5-5 mg elemental phosphorus/kg IV over 6h. Give as
potassium or sodium phosphate (93 mg phosphate/mL and 4 mEq
Na+ or K+/mL). Do not mix calcium and phosphorus in same IV.
Hyperphosphatemia
I. Clinical manifestations of hyperphosphatemia: Hypotension, bradycardia,
arrhythmias, bronchospasm, apnea, laryngeal spasm, tetany, seizures,
weakness, psychosis, confusion.
II. Clinical evaluation of hyperphosphatemia
A. Exogenous phosphate administration: Enemas, laxatives, diphos
phonates, vitamin D excess.
B. Endocrine disturbances: Hypoparathyroidism, acromegaly, PTH
resistance.
C. Labs: Phosphate, SMA 12, calcium, parathyroid hormone. 24-hr urine
phosphate, creatinine.
146 Hyperphosphatemia
III. Therapy: Correct hypocalcemia, restrict dietary phosphate, saline diuresis.
A. Moderate hyperphosphatemia
1. Aluminum hydroxide (Amphojel) 5-10 mL or 1-2 tablets PO ac tid;
aluminum containing agents bind to intestinal phosphate, and
decreases absorption OR
2. Aluminum carbonate (Basaljel) 5-10 mL or 1-2 tablets PO ac tid OR
3. Calcium carbonate (Oscal) (250 or 500 mg elemental calcium/tab) 1-2
gm elemental calcium PO ac tid. Keep calcium-phosphate product
<70; start only if phosphate <5.5.
B. Severe hyperphosphatemia
1. Volume expansion with 0.9% saline 1 L over 1h if the patient is not
azotemic.
2. Dialysis is recommended for patients with renal failure.
References
Al-Shamadi SM, Cameron EC, Sutton RA, AW. J. Kidney Dis 1994; 24:737-52
diabetic coma. Baillieres Clin Endo and Metab, Jan, 6(1):1, 1992.
Therapeutic Range*
Peak 25-30; trough <10 mcg/mL
1.0-3.0 mcg/mL
100-250 ng/mL
4-10 mcg/mL
150-300 ng/mL
0.8-2.0 ng/mL
2-5 mcg/mL
75-200 ng/mL
0.2-1.0 mcg/mL
Gentamicin . . . . . . . . . . . .
Imipramine . . . . . . . . . . . .
Lidocaine . . . . . . . . . . . . .
Lithium . . . . . . . . . . . . . . .
Nortriptyline . . . . . . . . . . .
Phenobarbital . . . . . . . . . .
Phenytoin** . . . . . . . . . . . .
Procainamide . . . . . . . . . .
Quinidine . . . . . . . . . . . . .
Salicylate . . . . . . . . . . . . .
Theophylline . . . . . . . . . . .
Valproic acid . . . . . . . . . . .
Vancomycin . . . . . . . . . . .
150-300 ng/mL
2-5 mcg/mL
0.5-1.4 mEq/L
50-150 ng/mL
10-30 mEq/mL
8-20 mcg/mL
4.0-8.0 mcg/mL
2.5-5.0 mcg/mL
15-25 mg/dL
8-20 mcg/mL
50-100 mcg/mL
* The therapeutic range of some drugs may vary depending on the reference lab
used.
** Therapeutic range of phenytoin is 4-10 mcg/mL in presence of significant
azotemia and/or hypoalbuminemia.
Index
Abacavir 85
Abciximab 31
Abelcet 86
Accolate 60
Accupril 34
Acetate 19
ACLS 5
Activated protein C 89
Acyclovir 85
AeroBid 59, 64
AeroBid-M 64
Agenerase 85
Aggrastat 31
Aggrenox 119
Albuterol 59, 63
Aldactone 34
Altace 34
Alteplase 29, 57
Alveolar/arterial O2 gradient
142
Amidate 49
Amikacin 82, 90
Amikin 90
Amino acid 19
Amino acid solution 19
Aminocaproic acid 74
Aminosyn 19
Amiodarone 40, 41, 45
Amoxicillin 65
Amoxicillin/Clavulanate 65, 81
Amphojel 141
Amphotericin B 86
Amphotericin B lipid complex
86
Ampicillin/Sulbactam 82, 90,
91
Amprenavir 85
Anectine 49
Angiodysplasia 97, 98
Angiography 98
Angiotensin-receptor blockers
34
Anion gap acidosis 125
Anticholinergic Crises 109
Anticholinergic Poisoning 106
Antidepressant Overdose 109
Antiretroviral Therapy 85
Antizol 110
Aredia 140
Arfonad 44
Arterial Line 21
Aspirin 27, 28, 119
Assist control 50
Asthma 58
Atacand 34
Atenolol 29-31
Ativan 51, 123
Atracurium 52
Atrial fibrillation 36
Augmentin 65, 81
Avapro 34
Azithromycin 65, 81, 86
Azmacort 59, 64
AZT 85
Bactrim 65, 84
Barbiturate coma 121
Basaljel 141
nation 15
Betapace 41, 45
Crixivan 85
Biaxin 65, 81, 86
Cromolyn 60, 61
Bisoprolol 35
Famotidine 94
Famotidine 20
Fat Emulsion 19
71
Feeding tubes 21
Fenoldopam 44
Fentanyl 49
Fibrinolytics 27
Flagyl 90
Flecainide 40, 45
Flovent 59
Flovent Rotadisk 59
Floxin 81, 82
Fluconazole 85, 86
Fluids 18
Flumazenil 102
Flunisolide 59, 64
Fluticasone 59
Fomepizole 110
Fortaz 82, 90
Foscarnet 85
Fosinopril 34
Fosphenytoin 123
Fragmin 30
Fresh Frozen Plasma 18
Fungizone 86
Furosemide 34, 36, 129, 132,
136
Gamma
Hydroxybutyrate
(GHB) 111
Ganciclovir 85, 86
Gastric Lavage 105
Gastrointestinal Bleeding 93,
96
Gentamicin 46, 82, 90, 92
Glomerulonephritis 128
Glycoprotein IIb/IIIa inhibitors
31
GoLytely 97
Heart failure 32
Hematochezia 96
Hematuria 129
Hemodialysis 106
Hemolytic Transfusion Reac
tion 71
Hemoperfusion 106
Hemorrhoid 98
Heparin 28, 30, 56
Hepatic Encephalopathy 102
Herpes simplex 85
Herpes Simplex Encephalitis
85
Herpes varicella zoster 85
High-dose penicillin G 82
Histoplasmosis 86
History 15
Hivid 85
Hydralazine 34, 44
Hydrochlorothiazide 34
Hyperaldosteronism 43
Hypercalcemia 139
Hypercalcemic Crisis 139
Hyperkalemia 130
Hypermagnesemia 135
Hypernatremia 138
Hyperphosphatemia 141
Hypertensive Emergencies 41
Hypertensive Emergency 41
Hypertensive Urgency 42
Hyperventilation 121
Hypokalemia 133
Hypomagnesemia 134
Hyponatremia 136, 137
Hypophosphatemia 140, 141
Ibuprofen 46
Ibutilide 40, 41
Imdur 31
Imipenem/cilastatin 90-92
Imodium 20
Metoclopramide 20
Inderal 39
Metolazone 34
Indinavir 85
Indocin 46
Metronidazole 90
Indomethacin 46
Mexiletine 45
INH 86
Mexitil 45
Mezlocillin 90
Intal 60, 61
Miacalcin 140
Integrilin 31
Milrinone 36
lation 53
Inter nal
jugular
vein Monopril 34
Montelukast 59, 60
cannulation 22
Morphine 26, 51
Intralipid 19
Motrin 46
Intropin 36
Mucomyst 107
Intubation 49
Inverse Ratio Ventilation 52 Multi-Trace Element For
mula 19
Invirase 85
Multiple organ dysfunction
Irbesartan 34
syndrome 87
Iron Overdose 111
Mycelex 85
Ischemic Colitis 98
Mycobacterium Avium Com
Ischemic Stroke 117
plex 86
Isoniazid 86
Isopropyl Alcohol Ingestion Mycobutin 86
Myocardial infarction 25
112
Myoglobin 26
Isoproterenol 45
N-Acetyl-Cysteine 107
Isoptin 38
Nafcillin 46
Isordil 31, 34
Narcotic Poisoning 106
Isosorbide 34
Nasogastric Tubes 21
Isosorbide dinitrate 31
Isosorbide mononitrate 31 Nasotracheal Intubation 50
Natrecor 36
Isuprel 45
Natriuretic peptides 36
Itraconazole 86
Nedocromil 60, 61
Jevity 20
Nelfinavir 85
Kaopectate 20
Neo-Synephrine) 50
Kayexalate 130, 132
Neomycin 103
Kefurox 82
Nesiritide 36
Ketoconazole 85
Neutral phosphate (NutraKetorolac 46
Phos) 141
Kussmaul's sign 69
Nevirapine 85
Labetalol 43
New York Heart Association
Lactulose 103
Criteria 33
Lamivudine 85
Nicardipine 44
Lanoxin 39
Nimbex 52
Lasix 34, 36, 132
Nipride 43
Levalbuterol 59
Nitrates 29
Levaquin 65, 81, 82, 92
Levofloxacin 65, 81, 82, 92 Nitroglycerin 26, 43
Nitroglycerin patch 31
Lidocaine 45
Nitroglycerin sublingual 31
Linezolid 90
Nitroglycerine 29, 36
Linton-Nachlas tube 95
Nitroglycerine aerosol 31
Lisinopril 29, 34
Nitroprusside 43
Lithium Overdose 112
Nizoral 85
Lomotil 20
Non-anion gap acidosis 125
Loperamide 20
NonQ-wave MI 25
Lopressor 29-31, 35, 39
NonQ-wave myocardial
Lorazepam 51, 123
infarction 30
Losartan 34
Norcuron 51
Lovenox 30
Low-molecular-weight hepa Norepinephrine 89, 115
Normodyne 43
rin 57
Lower
Gastrointestinal Norvir 85
NTG 31
Bleeding 96
Lung volume reduction sur Nutra-Phos 141
Octreotide 95, 102
gery 65
Ofloxacin 81, 82
Magnesium 19, 126, 135
Oliguria 127
Magnesium oxide 135
Oral Candidiasis 85
Magnesium sulfate 44
Mallory-Weiss Syndrome 94 Orotracheal Intubation 49
Osmolality, estimate of 142
Mannitol 121
Osmolite 20
Maxair 63
Oxacillin 46
Maxipime 91
Pacemakers 46, 47
Mefoxin 90
Packed Red Blood Cells 18
Melena 96
Pamidronate disodium 140
Meningitis 75
Pancreatitis 99
Meropenem 82, 90
Pancuronium 52
Merrem 82, 90
Paracentesis 91
Metabolic acidosis 125
Parenteral Nutrition 19
Methanol Ingestion 113
Pavulon 52
Methylprednisolone 61
Pentamidine 84
Pepcid 20, 94
vention 29
Pericardiocentesis 46, 69
Pericarditis 45
Peri pheral
Parenteral
Supplementation 19
Peritonitis 91
Phenobarbital 123
Phentolamine 44
Phenylephrine 89, 115
Phenytoin 45, 123
Phosphate 19, 126, 141
Physical Examination 15
Piperacillin 90
Piperacillin/tazobactam 82,
90-92
Pirbuterol 63
Pitressin 95
Platelets 18
Plavix 27, 119
Pleural Effusion 65
Pneumocystis carinii pneumo
nia 83
Pneumonia 79
Pneumothorax 67
Poisoning 105
Polyethylene glycol-electrolyte
solution 97
Postural hypotension 93
Potassium 19, 126
PRBC 18
Prednisolone 61
Prednisone 46, 61, 84
Pressure Support Ventilation
53
Primacor 36
Primaxin 90-92
Prinivil 29, 30, 34
Procainamide 39, 40, 44
ProCalamine 19
Procedure Note 17
Progress Note 17
Promix 20
Propafenone 40, 41, 45
Propofol 49, 51, 123
Propranolol 39
Protein powde 20
Proventil 59, 63
Pseudohyperkalemia 131
Pseudohyponatremia 136
Pulmicort 59, 64
Pulmocare 20
Pulmonary artery catheter 20
Pulmonary
Artery
Catheterization 23
Pulmonary artery pressure 24
Pulmonary embolism 54
Purulent Pericarditis 46
Pyrazinamide 86
Pyridoxine 86, 110
Pyrimethamine 86
Q-wave myocardial infarction
25
Quinapril 34
Quinidine 39, 40
Quinupristin/dalfopristin 90
Radiofrequency catheter abla
tion 41
Radiographic Evaluation 20
Radionuclide scan or bleeding
scan 97
Ramipril 34
Ranitidine 20, 94
Ranson's criteria 101
Reglan 20
Renal failure 127
ReoPro 31
Reperfusion therapy 27
Tocainide 45
Rescriptor 85
Tonocard 45
Respiratory Failure 50
Toradol 46
Reteplase 30
Torsades de pointes 44
Retitine 44
Torsemide 34
Retrovir 85
Rifabutin 86
Toxicology 105
Ringer's lactate 69
Toxoplasmosis 86
Ritonavir 85
tPA 30, 57
Romazicon 102
Tracheostomies 21
Rythmol 45
Tracrium 52
Transfusion reaction 71
Transjugular Intrahepatic
Sandostatin 95
Portacaval Shunt 95
Saquinavir 85
Secondary Hypertension 42
Trauma 67
Triamcinolone 59, 64
Sepsis 87, 89
Tricyclic antidepressant
Septic shock 87
overdose 109
Septra 65, 84
Trimethaphan 44
Serevent 59, 63, 64
Trimethoprim/SMX 65, 84
Sildenafil 29
Tr i me t h o pri m/sul fa
Singulair 59, 60
methoxazole 81
Slo-Bid 60
Troponin 26, 33
Slo-Mag 135
Tuberculosis 86
Sodium 19, 126, 136
in aids 86
Sodium Bicarbonate 132
Sodium
p o l y s t y r e n e
Type and Cross Match 18
sulfonate 130, 132 Type and Screen 18
Unasyn 82, 90, 91
Solu-Medrol 61
Unfractionated heparin 56
Sotalol 40, 41, 45
Unidur 60
Spironolactone 34
Unstable angina 25, 30
Sporanox 86
Spot urine sodium concen Upper Gastrointestinal
Bleeding 93
tration 129
ST-segment depression 25 Urinalysis 129
ST-segment elevation infarc Valacyclovir 85
Valsartan 34
tion 25
Valtrex 85
Starvation ketosis 125
Vanceril 59
Status Epilepticus 122
Vancocin 82
Stavudine 85
Vancomycin 46, 82, 90
Streptase 29
Va n c o my c i n - r e s i s t a n t
Streptokinase 29
enterococcus 90
Stroke 117
Subclavian vein cannulation Variceal 95
Variceal bleeding 94
23
Variceal hemorrhage 95
Sublimaze 49
Varicella 85
Succinylcholine 49
Vasopressin 95
Sulfadiazine 86
Vasotec 34, 44
Sulfonamide 81
Vecuronium 51
Sustiva 85
Sympathomimetic Poisoning Ventilation-perfusion Scan
55
106
Ventilator Management 50,
Synercid 90
51
Systemic inflammatory re
sponse syndrome 87 Ventilator Weaning 52
Ventolin 59, 63
t-PA 29, 117
Ventricular arrhythmias 44
Tagamet 94
Ventricular fibrillation 44
Tambocor 45
Ventricular tachycardia 44
Tamponade 69, 95
Verapamil 38
Tenectaplase 30
Versed 49-51, 123
Tenormin 29-31
Tension Pneumothorax 68 Viagra 29
Vibramycin 65
Tetracycline 81
Videx 85
Theo-Dur 60
Viramune 85
Theophylline 60, 61, 64
Vitamin B 12 19
Theophylline Toxicity 114
Vitamin K 19, 115
Thiamine 123
Thrombolytic-associ ated Warfarin 57
Warfarin overdose 115
Bleeding 73
Water excess 139
Thrombolytics 28
Weaning Protocols 53
Ticarcillin 90
Ticarcillin/clavulanate 82, Whole Bowel Irrigation 105
Withdrawal Syndrome 106
90-92
Wymox 65
Tikosyn 41
Xopenex 59
Tilade 60, 61
Zafirlukast 60
Timentin 82, 90-92
Zalcitabine 85
Tirofiban 31
Tissue plasminogen activator Zantac 20, 94
Zaroxolyn 34
29, 57, 117
Zebeta 35
Tobramycin 46, 90, 92
Zerit 85
Zestril 34
Ziagen 85
Zidovudine 85
Zileuton 60, 61
Zinacef 82
Zoster 85
Zovirax 85
Zyflo 60, 61
Zyvox 90
Medicine, 2001Edition
2002 Edition
Surgery, 2002 Edition
Pediatric Drug Reference, 2002 Edition
Critical Care Medicine, 2002-2003 Edition
Psychiatry, 2002 Edition
Pediatrics, 2002 Edition
Physicians Drug Manual, 2001 Edition
Pediatric History and Physical Examination, Fourth Edition